Podcasts about macrophages

A new experiment shows pigeons use immune cells to navigate our planet. The discovery redefines our understanding of how an animal can 'feel' Earth's magnetic field.

Guest: Dr. Filipa Simões is a Group Leader at the University of Oxford and Co-Director of the Oxford Organoid Hub. She discusses how macrophages shape heart development, repair, and regeneration, and how cellular crosstalk within the cardiac niche influences tissue outcomes after injury. Using zebrafish models, stem cell–derived cardiac organoids, and spatial genomics approaches, she explores the molecular signals that govern macrophage identity and function, with the goal of uncovering new strategies to promote cardiac regeneration and limit fibrosis. Featured Products and Resources: Join us at ISSCR and discover the breakthroughs and technologies you can take straight back to your lab. Enter to win 350 US dollars or equivalent towards refreshments to fuel your next journal club. The Stem Cell Science Round Up iPSC Therapy for Heart Failure – Engineered heart muscle grafts derived from iPSCs increased heart wall thickness and improved cardiac function in patients with heart failure. Inflammatory Memory in HSCs – A distinct human HSC subset retains inflammatory memory, influencing blood production, aging, and disease risk. Organoid-Mediated Vision Recovery – Transplanted human retinal organoids partially restored vision after complete optic nerve transection in rats. Improving HSPC Gene Therapy – A new selection strategy enriches precisely edited hematopoietic stem cells while reducing unwanted genomic alterations. Photo Reference: Courtesy of Filipa Simões. Subscribe to our newsletter! Never miss updates about new episodes. Subscribe

Send us Fan MailIs the fundamental purpose of sleep to remove oxidized fats from the brain?Nick & Dr. Amita Sehgal talk about the latest science on why animals sleep. Using fruit flies, her lab shows that waking generates oxidized lipids in neurons that are shuttled to glia and then cleared by macrophage-like cells during sleep. This process protects mitochondria, supports memory, and links sleep to metabolic cleanup rather than just rest.TOPICS DISCUSSED:Drosophila as a model: Fruit flies sleep with immobility, reduced responsiveness, and homeostatic rebound; their genetics reveal conserved mechanisms found in humans.Circadian vs homeostatic sleep: Circadian timing sets when we sleep; homeostatic drive builds need from prolonged wakefulness independent of time of day.Metabolic waste during wake: Neuronal activity oxidizes lipids in mitochondria; these damaged lipids transfer to glial support cells via apolipoproteins.Immune cells clear brain trash: Macrophage-like hemocytes dock at the brain during sleep, phagocytose oxidized lipids, and remove them; blocking this docking reduces sleep and impairs memory.Peroxisomes & oxidative stress: These organelles handle specific fats and rise with wakefulness; disrupting them increases brain oxidation that can be partially rescued by antioxidants like N-acetylcysteine.Sickness sleep differs from normal sleep: Infection-induced sleep redirects energy to immune defense and depletes rather than restores brain energy stores.ABOUT THE GUEST: Amita Sehgal, PhD is the John Herr Musser Professor of Neuroscience at the University of Pennsylvania, an HHMI Investigator, and director of the Chronobiology and Sleep Institute. She uses Drosophila genetics to uncover basic mechanisms of circadian rhythms and sleep.RELATED EPISODE:M&M 257: Sleep, Mitochondrial Metabolism & Oxidative Stress | Gero MiesenbockSupport the showHealth Products by M&M Partners:SporesMD: Premium mushrooms products (gourmet mushrooms, nootropics, research). Use code 'nickjikomes' for 20% off.Lumen device: Optimize your metabolism for weight loss or athletic performance. MINDMATTER gets you 15% off.AquaTru: Water filtration devices that remove microplastics, metals, bacteria, and more from your drinking water. Through link, $100 off AquaTru Carafe, Classic & Under Sink Units; $300 off Freestanding models.Seed Oil Scout: Find restaurants with seed oil-free options, scan food products to see what they're hiding, with this easy-to-use mobile app.KetoCitra—Ketone body BHB + electrolytes formulated for kidney health. Use code MIND20 for 20% off any subscription (cancel anytime)For all the ways you can support my efforts

SRP Researchers developed an advanced cell culture model that better represents the human lung.

Dr. Niyati Borkar chats with Dr. Marissa Guttenberg about her article, "Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK-mediated Efferocytosis."

Dr. Petri Bono, Chief Medical Officer at Faron Pharmaceuticals, describes the development of bexmarilimad, a novel first-in-class immunotherapy that, unlike existing checkpoint inhibitors targeting T cells, targets the Clever 1 receptor on macrophages. This treatment is designed to reprogram the tumor microenvironment by switching marcophages from suppressive to active, enabling the patient's immune system to recognize and attack cancer cells. The primary disease target is higher-risk Myelodysplastic syndromes because the cancer cells in virtually all MDS patients express the Clever 1 target. Petri explains, "We are developing a completely new type of treatment. Currently, cancer patients are treated with immunotherapies called checkpoint inhibitors that target immune checkpoints. But our approach is targeting completely different cells, not T cells, but rather macrophages. And that's why we are first in class with a novel mode of action. And that's why it's important that these macrophages are shown to, for example, contribute to treatment resistance in many tumors." "Clever 1 actually is a receptor that was identified about 20 years ago. It found a certain macrophage as well as myeloid cells. And Clever 1 keeps the immune system in a tolerant and suppressive state. In cancer, for example, these Clever 1-positive macrophages essentially help the malignancy grow instead of helping to fight against it. And then our approach is that we want to block Clever 1 with our monoclonal antibody, bexmarilimab. So those macrophages switch the phenotype into an active antigen, preventing a pro-inflammatory state, and this reawakens immune surveillance. It allows T cells in the system to actually recognize the malignant cells themselves as dangerous and mount a proper antitumor response. So, a completely new mode of action by targeting Clever 1, we are not just adding another cytotoxic mechanism. We are removing the immune break and enabling the patient's own immune system to do the job that it was originally designed to do."  #FaronPharmaceuticals #BloodCancer #MDS #MyelodysplasticSyndrome #HR-MDS #CancerResearch #novelimmunotherapy #Bexmarilimab #Clever1 faron.com Download the transcript here

Dr. Petri Bono, Chief Medical Officer at Faron Pharmaceuticals, describes the development of bexmarilimad, a novel first-in-class immunotherapy that, unlike existing checkpoint inhibitors targeting T cells, targets the Clever 1 receptor on macrophages. This treatment is designed to reprogram the tumor microenvironment by switching marcophages from suppressive to active, enabling the patient's immune system to recognize and attack cancer cells. The primary disease target is higher-risk Myelodysplastic syndromes because the cancer cells in virtually all MDS patients express the Clever 1 target. Petri explains, "We are developing a completely new type of treatment. Currently, cancer patients are treated with immunotherapies called checkpoint inhibitors that target immune checkpoints. But our approach is targeting completely different cells, not T cells, but rather macrophages. And that's why we are first in class with a novel mode of action. And that's why it's important that these macrophages are shown to, for example, contribute to treatment resistance in many tumors." "Clever 1 actually is a receptor that was identified about 20 years ago. It found a certain macrophage as well as myeloid cells. And Clever 1 keeps the immune system in a tolerant and suppressive state. In cancer, for example, these Clever 1-positive macrophages essentially help the malignancy grow instead of helping to fight against it. And then our approach is that we want to block Clever 1 with our monoclonal antibody, bexmarilimab. So those macrophages switch the phenotype into an active antigen, preventing a pro-inflammatory state, and this reawakens immune surveillance. It allows T cells in the system to actually recognize the malignant cells themselves as dangerous and mount a proper antitumor response. So, a completely new mode of action by targeting Clever 1, we are not just adding another cytotoxic mechanism. We are removing the immune break and enabling the patient's own immune system to do the job that it was originally designed to do."  #FaronPharmaceuticals #BloodCancer #MDS #MyelodysplasticSyndrome #HR-MDS #CancerResearch #novelimmunotherapy #Bexmarilimab #Clever1 faron.com Listen to the podcast here

With Marie-Noelle Giraud, Faculty of Science and Medicine, Fribourg - Switzerland and Carolina Balbi, Research Centre for Molecular Biology, University of Zurich - Switzerland. Link to European Heart Journal paper Link to European Heart Journal editorial

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In this inspiring episode, Dr. Felipe Gálvez-Cancino, group leader at Oxford's Center for Immuno-Oncology, walks us through his team's groundbreaking research on macrophages, T cells, and immune regulation in solid tumors. Tracing his path from early cancer vaccine work to advanced antibody-dependent cellular phagocytosis (ADCP), Felipe shares how his team is working to reprogram tumor-associated macrophages to more efficiently eliminate cancer cells.He explains how regulatory CD4+ T cells suppress both T cell and macrophage responses within tumors and how removing that suppression can supercharge phagocytic function. We also hear how his lab is leveraging mouse models of hepatocellular carcinoma, clinical samples, and modern molecular biology techniques (like in vivo liver transfection and CRISPR-ready plasmid engineering) to study intratumor heterogeneity and antigen spreading.Felipe also reflects on the value of early molecular biology training—like mastering gigapreps—and emphasizes the importance of curiosity, persistence, and collaboration in scientific careers. Whether you're interested in cancer biology, immunotherapy, or just passionate about translating discoveries into new therapies, this episode offers both technical depth and motivational insight. Subscribe to get future episodes as they drop and if you like what you're hearing we hope you'll share a review or recommend the series to a colleague.  Visit the Invitrogen School of Molecular Biology to access helpful molecular biology resources and educational content, and please share this resource with anyone you know working in molecular biology. For Research Use Only. Not for use in diagnostic procedures.

Send us a textThe surprising link between oral bacteria and heart disease.Episode Summary: Dr. Pekka Karhunen explains the connection between oral bacteria, cholesterol, and cardiovascular disease, discussing how oxidized LDL cholesterol triggers inflammation in arteries, how bacteria from the mouth can infiltrate arterial plaques to form biofilms, and the implications for heart disease prevention through lifestyle changes like better oral hygiene.About the guest: Pekka Karhunen, MD, PhD is a medical doctor and forensic pathologist with decades of experience, specializing in cardiovascular diseases. He has created a unique biobank of coronary arteries from over 10,000 autopsies conducted in Finland. His research focuses on the role of bacteria in atherosclerosis, particularly through studying coronary artery plaques.Discussion Points:Cholesterol is essential for life, but oxidized low-density lipoprotein (LDL) cholesterol is seen as a foreign substance by the immune system, leading to chronic inflammation in coronary arteries.Macrophages ingest oxidized LDL, turning into dysfunctional foam cells that contribute to plaque buildup, known as atheromas, in arteries.Plaque rupture, potentially caused by increased pressure from cholesterol accumulation or hemorrhage within the plaque, can trigger heart attacks.Bacteria, especially from the mouth, can enter arterial plaques via bacteremia (e.g., from dental procedures) and form biofilms, evading immune detection.Biofilms in plaques, made of extracellular matrix like polysaccharides, protect bacteria and may contribute to plaque instability or calcification over time.Poor oral hygiene is linked to higher cardiovascular disease risk, as bacteria from dental infections can enter plaques, suggesting dental care as a preventive measure.Karhunen's research found oral bacteria, like Viridans streptococci, in coronary plaques, with unpublished data also detecting gut and skin bacteria, indicating diverse bacterial involvement.Related content:M&M 247: Cholesterol: Immune Benefits, Heart Health, Statins & Research Malpractice | Uffe Ravnskov*Not medical advice.Support the showAffiliates: Seed Oil Scout: Find restaurants with seed oil-free options, scan food products to see what they're hiding, with this easy-to-use mobile app. KetoCitra—Ketone body BHB + electrolytes formulated for kidney health. Use code MIND20 for 20% off any subscription (cancel anytime) Lumen device to optimize your metabolism for weight loss or athletic performance. Code MIND for 10% off SiPhox Health—Affordable at-home blood testing. Key health markers, visualized & explained. Code TRIKOMES for a 20% discount. For all the ways you can support my efforts

Dr. Eric Morrell sits down with Dr. Maude Liegeois to discuss her paper, "Airway Macrophages Encompass Transcriptionally and Functionally Distinct Subsets Altered by Smoking."

Dr. Peter Moore chats with Dr. Marilia Zuttion on her article, "Interstitial Macrophages Mediate Efferocytosis of Alveolar Epithelium during Influenza Infection."

Diagnosed at just 15, Zac opens up about the difficult shift from being an active athlete to facing disability caused by arthritis and its complications. He shares how strength training became a turning point and helped him regain mobility, lose weight, and rebuild a fulfilling life. He also explores how his background in strength training helped him survive a near death experience with macrophage activation syndrome.Together, Cheryl and Zac explore the role of exercise in managing arthritis, offering practical tips, tools, and encouragement for others navigating similar challenges. Zac highlights the importance of pairing medical treatment with disciplined strength training to enhance both health and quality of life.Episode at a glance:Zac's Diagnosis Journey: Zac Spinosa, 28-year-old personal trainer living with Juvenile Idiopathic Arthritis (JIA), shares the challenges of shifting from active athlete to living with disability. Turning Point: How strength training helped Zac regain mobility, lose weight, and rebuild his lifePractical Takeaways: Tips, tools, and advice for using exercise to manage arthritis effectivelyHolistic Approach: The importance of combining medical treatment with disciplined strength trainingInspiration for Listeners: Finding resilience, strength, and quality of life while navigating chronic illnessMedical disclaimer: All content found on Arthritis Life public channels was created for generalized informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment.Episode SponsorsRheum to THRIVE, an online course and support program Cheryl created to help people with rheumatic disease go from overwhelmed, confused and alone to confident, supported and connected. See all the details and join the program or waitlist now! 

Send us a textCellular clean up by immune cells and how early-life fructose exposure leads to neurodevelopmental problems.Episode Summary: Dr. Justin Perry talks about the body's constant cellular turnover—about 3 million cells die per second in adults (double in children and women)—handled by phagocytes like macrophages that engulf and digest debris to prevent diseases like lupus. They explore phagocytosis steps, macrophage adaptations in tissues like the brain (microglia), and how high fructose intake impairs microglial function in developing mice, leading to uncleared brain cells and anxiety-like behaviors, with implications for human neurodevelopmental disorders amid rising fructose consumption.About the guest: Justin Perry, PhD is an immunologist and clinical psychologist who leads a lab at Memorial Sloan Kettering Cancer Center focusing on how the body clears dead cells and debris to maintain homeostasis.Discussion Points:The body turns over 1-2% of its 30 trillion cells daily, mostly blood cells, but neurons in kids and endometrium in women turnover at ~2x this ratePhagocytosis involves "find me," "eat me," and digestion signals; failures can cause autoimmunity.Microglia are brain macrophages that uptake fructose via GLUT5 transporter.Early high fructose exposure (comparable to one soda daily) impairs the pruning of synapses and dead neurons.In mice, prenatal or postnatal fructose causes phagocytosis deficits in the prefrontal cortex, leading to heightened fear responses and poor fear extinction, mimicking anxiety disorders.Fructose correlates with rising neurodevelopmental issues like autism and anxiety; it's passed via breast milk, and liquid forms (e.g., sodas) overwhelm metabolic shields more than solid fruits.Macrophages may hold keys to diseases from atherosclerosis to cancer; deleting GLUT5 in microglia reverses fructose's effects, hinting at evolutionary roles in aging or low-oxygen states.Related content:M&M 215: Cancer Metabolism: Sugar, Fructose, Lipids & Fasting | Gary PattiArticle | Dietary Fructose & Metabolic Health: An Evolutionary PerspectiveReference Paper:Study | Early life high fructose impairs microglial phagocytosis and neurodevelopment*Not medical advice.Support the showAffiliates: Seed Oil Scout: Find restaurants with seed oil-free options, scan food products to see what they're hiding, with this easy-to-use mobile app. KetoCitra—Ketone body BHB + electrolytes formulated for kidney health. Use code MIND20 for 20% off any subscription (cancel anytime) Lumen device to optimize your metabolism for weight loss or athletic performance. Code MIND for 10% off SiPhox Health—Affordable at-home blood testing. Key health markers, visualized & explained. Code TRIKOMES for a 20% discount. For all the ways you can support my efforts

In this encore episode, we detail the gut-immune axis, focusing on the protective mucus layer and the roles of secretory immunoglobulin A and lactoferrin in intestinal health. We discuss endogenous secretions as well as highlight lactoferrin testing and levels. Topics: 1. The Intestinal Barrier & Mucus Layer- The intestinal lumen, microbiome, mucus layer, epithelial cells, and lamina propria.- The mucus layer: antimicrobial peptides (AMPs) and secretory IgA (sIgA).- Intestinal epithelial cells including goblet cells and enterocytes.2. Immune Cells in the Gut- The lamina propria.- Macrophages, dendritic cells, neutrophils, B cells, T cells, mast cells, and more.3. Antimicrobial Peptides & Secretory IgA- AMPs and sIgA in the mucus layer aid in regulating microbial balance and pathogen adhesion.4. Lactoferrin: Functions & Sources- Iron-binding glycoprotein, antimicrobial and immunomodulatory properties.- Found in mucosal secretions, colostrum, and more.- Intestinal epithelial cells (IECs) and neutrophils.5. Lactoferrin's Role in Intestinal Health- Regulates iron absorption via lactoferrin receptors (LFR)on enterocytes.- Sequesters free iron, limiting bacterial growth, bacteriostatic.- Destabilizes bacterial membranes, cell lysis, bactericidal.6. Lactoferrin Levels- Neutrophils release lactoferrin during infection,increasing its presence in the large intestine.- Fecal lactoferrin levels.- Fecal calprotectin levels.7. Candida Overgrowth8. Lactoferrin Supplementation to Support the Gut9. Conclusion- The intestinal mucus layer.- Lactoferrin.Thank you to our episode sponsor: 1. ⁠⁠⁠OmneDiem®'s⁠⁠⁠ ⁠⁠⁠Histamine Digest®⁠⁠⁠ and ⁠⁠⁠Histamine Digest® PureMAX⁠⁠⁠ 2. ⁠⁠⁠Histamine Digest® Histamine Complete⁠⁠⁠ with DAO, Vitamin C, Quercetin, Bromelain, and Stinging Nettle Root Extract.Thanks for tuning in!Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠

In this week's episode we'll learn more about enhanced transplant characteristics; targeting the JAK-STAT pathway with ruxolitinib in patients with adult-onset Still's disease and macrophage activation syndrome; and a pair of trials demonstrating lack of benefit for the anti-CD47 monoclonal antibody magrolimab in newly diagnosed acute myeloid leukemia.Featured ArticlesHeterogeneity of high-potency multilineage hematopoietic stem cells and identification of “Super” transplantabilityRuxolitinib targets JAK-STAT signaling to modulate neutrophil activation in refractory macrophage activation syndromeMagrolimab plus azacitidine vs physician's choice for untreated TP53-mutated acute myeloid leukemia: the ENHANCE-2 studyThe ENHANCE-3 study: venetoclax and azacitidine plus magrolimab or placebo for untreated AML unfit for intensive therapy

Broadcast from KSQD, Santa Cruz on 6-26-2025: Dr. Dawn opens with groundbreaking results from Vertex Pharmaceuticals' stem cell treatment for severe type 1 diabetes. The experimental therapy, Zimislecel, converts stem cells into pancreatic islet cells and infuses them into patients. In a 12-person study, 10 patients no longer need insulin after one year. The cells migrated to the liver and began producing insulin in response to glucose levels. Patients with hypoglycemic unawareness saw complete elimination of dangerous episodes after three months. However, patients must take lifelong immunosuppressive drugs to prevent rejection. The research represents 25 years of work by Harvard's Doug Melton. A caller asks about Keytruda treatment for melanoma. Dr. Dawn explains it's an immunotherapy drug targeting programmed death receptors that cancer cells hijack to evade immune response. The drug can cause serious immune overreactions but is standard for metastatic melanoma. Treatment protocols depend on cancer staging. For young patients with decades to lose, aggressive treatment is often justified despite risks. An email about morning arthritis pain leads to chronotherapy research discussion. Macrophages have energy levels that peak in the morning when inflammasome activation is quicker and more robust, explaining why arthritis pain is worst after overnight rest. Treatment timing could optimize anti-inflammatory medications by taking them at bedtime. Another email about eye irritation prompts diagnostic discussion. Dr. Dawn recommends examining for bacterial blepharitis before assuming food allergies and testing antihistamine drops. For elimination diets, common allergens include wheat, dairy, corn, soy, and peanuts. However, without other symptoms, food allergies are unlikely causes of isolated eye problems. Dr. Dawn explores advancing CAR-T cell therapy using RNA technology. Traditional therapy costs up to $500,000 per patient requiring lab reprogramming. New RNA-containing nanoparticles temporarily create antigen receptors for about one week. Mouse studies eliminated detectable tumors at highest doses. While effects are temporary, this could dramatically reduce costs and complexity. She discusses DNA forensics evolution from O.J. trial era to current technologies. New paleogenomics technology can analyze fragmented DNA from hair, previously considered unusable. Mitochondrial DNA analysis can definitively exonerate suspects. This led to Charles Fane's release after 17 years on death row when hair evidence proved innocence and identified the actual perpetrator. Dr. Dawn introduces Barrett's esophagus screening replacing invasive endoscopy. Patients swallow a capsule containing a compressed sponge that expands in the stomach and is pulled out via string, collecting esophageal cells. The test identifies abnormalities with 100-fold increased cancer risk when positive and 98% accuracy when negative, allowing targeted endoscopy only for high-risk patients. She concludes discussing body composition analysis superiority over BMI. Studies found overweight BMI showed 3.6 times higher heart disease risk, while large waist circumference showed four times higher risk. However, BMI had no significant relationship with overall mortality. Dr. Dawn advocates for bioimpedance analysis devices to measure body fat percentage and track muscle loss.

Broadcast from KSQD, Santa Cruz on 6-26-2025: Dr. Dawn opens with groundbreaking results from Vertex Pharmaceuticals' stem cell treatment for severe type 1 diabetes. The experimental therapy, Zimislecel, converts stem cells into pancreatic islet cells and infuses them into patients. In a 12-person study, 10 patients no longer need insulin after one year. The cells migrated to the liver and began producing insulin in response to glucose levels. Patients with hypoglycemic unawareness saw complete elimination of dangerous episodes after three months. However, patients must take lifelong immunosuppressive drugs to prevent rejection. The research represents 25 years of work by Harvard's Doug Melton. A caller asks about Keytruda treatment for melanoma. Dr. Dawn explains it's an immunotherapy drug targeting programmed death receptors that cancer cells hijack to evade immune response. The drug can cause serious immune overreactions but is standard for metastatic melanoma. Treatment protocols depend on cancer staging. For young patients with decades to lose, aggressive treatment is often justified despite risks. An email about morning arthritis pain leads to chronotherapy research discussion. Macrophages have energy levels that peak in the morning when inflammasome activation is quicker and more robust, explaining why arthritis pain is worst after overnight rest. Treatment timing could optimize anti-inflammatory medications by taking them at bedtime. Another email about eye irritation prompts diagnostic discussion. Dr. Dawn recommends examining for bacterial blepharitis before assuming food allergies and testing antihistamine drops. For elimination diets, common allergens include wheat, dairy, corn, soy, and peanuts. However, without other symptoms, food allergies are unlikely causes of isolated eye problems. Dr. Dawn explores advancing CAR-T cell therapy using RNA technology. Traditional therapy costs up to $500,000 per patient requiring lab reprogramming. New RNA-containing nanoparticles temporarily create antigen receptors for about one week. Mouse studies eliminated detectable tumors at highest doses. While effects are temporary, this could dramatically reduce costs and complexity. She discusses DNA forensics evolution from O.J. trial era to current technologies. New paleogenomics technology can analyze fragmented DNA from hair, previously considered unusable. Mitochondrial DNA analysis can definitively exonerate suspects. This led to Charles Fane's release after 17 years on death row when hair evidence proved innocence and identified the actual perpetrator. Dr. Dawn introduces Barrett's esophagus screening replacing invasive endoscopy. Patients swallow a capsule containing a compressed sponge that expands in the stomach and is pulled out via string, collecting esophageal cells. The test identifies abnormalities with 100-fold increased cancer risk when positive and 98% accuracy when negative, allowing targeted endoscopy only for high-risk patients. She concludes discussing body composition analysis superiority over BMI. Studies found overweight BMI showed 3.6 times higher heart disease risk, while large waist circumference showed four times higher risk. However, BMI had no significant relationship with overall mortality. Dr. Dawn advocates for bioimpedance analysis devices to measure body fat percentage and track muscle loss.

We catch up with Assistant Professor Sudarshan Dayanidhi!Muscle morphology and Macrophages: What can muscle morphology tell us about the progression of cerebral palsy, and how can this inform treatment approaches?Another brilliant interview with researchers from EACD / IAACD 2025 at Heidelberg Germany!

Vincent and Cindy discuss differences between MPox-specific T cell responses following infection and vaccination, and lymph node macrophage control of memory B cell localization and trafficking that might be important for choosing which arm to get a vaccine. Hosts: Vincent Racaniello and Cindy Leifer Subscribe (free): Apple Podcasts, RSS, email Become a patron of Immune! Links for this episode MicrobeTV Discord Server Different T memory response to MPox infection or vaccination (Nat Comm 2025) Macrophages direct B cell recall responses after vaccination (Cell 2025) Time stamps by Jolene Ramsey. Thanks! Music by Tatami. Immune logo image by Blausen Medical Send your immunology questions and comments to immune@microbe.tv Information on this podcast should not be construed as medical advice.

In this encore episode, we detail the gut-immune axis, focusing on the protective mucus layer and the role of lactoferrin in intestinal health. We discuss endogenous secretions and how lactoferrin functions as an antimicrobial, immunomodulatory, and iron-regulating glycoprotein, influencing microbial balance and intestinal barrier integrity. Additionally, we highlight lactoferrin testing and levels. We finish by going through supplementation as a phenomenal tool.Topics: 1. The Intestinal Barrier & Mucus Layer- The intestinal lumen, microbiome, mucus layer, epithelial cells, and lamina propria.- The mucus layer: antimicrobial peptides (AMPs) and secretory IgA (sIgA).- Intestinal epithelial cells including goblet cells and enterocytes.2. Immune Cells in the Gut- The lamina propria.- Macrophages, dendritic cells, neutrophils, B cells, T cells, mast cells, and more.3. Antimicrobial Peptides & Secretory IgA- AMPs and sIgA in the mucus layer regulate microbial balance and prevent pathogen adhesion.4. Lactoferrin: Functions & Sources- Iron-binding glycoprotein, antimicrobial and immunomodulatory properties.- Found in mucosal secretions, colostrum, and more.- Intestinal epithelial cells (IECs) and neutrophils.5. Lactoferrin's Role in Intestinal Health- Regulates iron absorption via lactoferrin receptors (LFR)on enterocytes.- Sequesters free iron, limiting bacterial growth, bacteriostatic.- Destabilizes bacterial membranes, cell lysis, bactericidal.6. Lactoferrin Levels- Neutrophils release lactoferrin during infection,increasing its presence in the large intestine.- Fecal lactoferrin levels.- Fecal calprotectin levels.7. Lactoferrin & Candida Overgrowth- Fungal membranes.- Aiding in the inhibition of biofilm formation.8. Lactoferrin Supplementation & Benefits- Supports gut microbiota, epithelial integrity, and immune modulation.- Bovine colostrum and as a supplement.9. Conclusion- The intestinal mucus layer is key to gut barrier function.- Lactoferrin plays a central role in microbial regulation and immune defense.Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠

Story at-a-glance Macrophages and mitochondria are immune partners; macrophages clear germs and control inflammation, while mitochondria power cells and signal macrophages to manage inflammation effectively Mitochondria's complex III produces superoxide, signaling macrophages to release IL-10, the "off switch" for inflammation — key for preventing chronic and autoimmune issues Research showed impaired mitochondrial complex III reduces IL-10, causing unchecked inflammation and severe illness, highlighting mitochondria's important immune regulatory role Naturally boost IL-10 through fiber-rich foods for butyrate, sunshine exposure, exercise and spices like garlic to enhance your body's inflammation control mechanisms Healthy mitochondria, threatened by seed oils in processed foods and toxins, are essential for energy and immunity; lifestyle choices significantly impact mitochondrial function and overall well-being

In this episode, we discuss the very early stages of drug targets and drug development with Dr. Mohd Shahid, PhD. Dr. Shahid's research involves the IER3 gene, which is an important modulator of the body's inflammatory response via its action in major immune cells, including macrophages and T-cells, and plays a role in metabolic disorders such as obesity, diabetes, and atherosclerosis, revealing a previously unknown function of this protein. Key Concepts Drug development is a multi-decade journey – human clinical trials occur very late in the process. Drug development often starts before a drug molecule is even conceived by identifying potential drug targets. Chronic inflammation is important for a variety of diseases, including obesity and atherosclerosis. Dr. Shahid's work focuses on a specific gene, Immediate Early Response 3 Gene (IER3 or IEX-1), and its role in modulating the inflammatory response in these disease states. The research process frequently leads to unexpected discoveries and new lines of inquiry. With Dr. Shahid, his work in obesity and inflammation actually led to a new understanding of the IER3's role in the interplay between macrophages, inflammation, and energy expenditure. References Shahid M, Javed AA, Chandra D, et al. IER3 deficiency induces browning of white adipose tissue and resists diet-induced obesity. Sci Rep. 2016;6:24135. Published 2016 Apr 11. doi:10.1038/srep24135 Shahid M, Hermes EL, Chandra D, et al. J Am Heart Assoc. 2018;7:e009261. DOI: 10.1161/JAHA.118.009261. Ridker PM, Danielson E, Fonseca FA, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359(21):2195-2207. doi:10.1056/NEJMoa0807646 Tardif JC, Kouz S, Waters DD, et al. Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction. N Engl J Med. 2019;381(26):2497-2505. doi:10.1056/NEJMoa1912388

In this episode, we detail the gut-immune axis, focusing on the protective mucus layer, antimicrobial peptides, and the role of lactoferrin in intestinal health. We discuss endogenous secretions and how lactoferrin functions as an antimicrobial, immunomodulatory, and iron-regulating glycoprotein, influencing microbial balance and intestinal barrier integrity. Additionally, we highlight lactoferrin testing and levels. We finish by going through supplementation as a phenomenal tool.Topics: 1. The Intestinal Barrier & Mucus Layer- The intestinal lumen, microbiome, mucus layer, epithelial cells, and lamina propria.- The mucus layer: antimicrobial peptides (AMPs) and secretory IgA (sIgA).- Intestinal epithelial cells including goblet cells and enterocytes.2. Immune Cells in the Gut- The lamina propria.- Macrophages, dendritic cells, neutrophils, B cells, T cells, mast cells, and more.3. Antimicrobial Peptides & Secretory IgA- AMPs and sIgA in the mucus layer regulate microbial balance and prevent pathogen adhesion.4. Lactoferrin: Functions & Sources- Iron-binding glycoprotein, antimicrobial and immunomodulatory properties.- Found in mucosal secretions, colostrum, and more.- Intestinal epithelial cells (IECs) and neutrophils.5. Lactoferrin's Role in Intestinal Health- Regulates iron absorption via lactoferrin receptors (LFR)on enterocytes.- Sequesters free iron, limiting bacterial growth, bacteriostatic.- Destabilizes bacterial membranes, cell lysis, bactericidal.6. Lactoferrin Levels- Neutrophils release lactoferrin during infection,increasing its presence in the large intestine.- Fecal lactoferrin levels.- Fecal calprotectin levels.7. Lactoferrin & Candida Overgrowth- Fungal membranes.- Aiding in the inhibition of biofilm formation.8. Lactoferrin Supplementation & Benefits- Supports gut microbiota, epithelial integrity, and immunemodulation.- Bovine colostrum and as a supplement.9. Conclusion- The intestinal mucus layer is key to gut barrier function.- Lactoferrin plays a central role in microbial regulationand immune defense.Thank you to our episode sponsors:1. Shop ⁠⁠⁠⁠Fresh Press Farms⁠⁠⁠'⁠⁠Peach Cider Vinegar⁠ at Sprouts locations nationwide, and check out their full collection ⁠⁠⁠⁠here⁠⁠⁠⁠. 2. Shop CYLN's full skincare line here.Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠

In this episode, we dive into the interplay between the gut microbiota (their postbiotics) and the immune system. We will examine how gut microbiome-derived metabolites, such as short-chain fatty acids (SCFAs) and polyphenol metabolites, influence immune function by modulating key cellular and molecular pathways within the intestinal mucosa. Additionally, we discuss strategies for supporting butyrate production and optimizing microbiome health to foster a balanced and resilient gut-immune axis. Topics: 1. Introduction Overview of the gut-immune axis. Importance of gut microbiome-derived metabolites in supporting immune function. 2. The Intestinal Barrier Layers of the intestinal wall Focus on mucosa, specifically the epithelium and lamina propria. 3. Structure of the Intestinal Layers The intestinal lumen, mucus layer, epithelium (with tight junctions), and lamina propria. Importance of the lamina propria as a hub for immune responses and structural integrity. 4. Cellular and Structural Components of the Lamina Propria Extracellular matrix (ECM): structural support. Fibroblasts and myofibroblasts. Lymphatic vessels: immune cell transport, linking mucosal and systemic immune systems. 5. Immune Cells in the Lamina Propria T cells: immune tolerance, regulatory T cells (Tregs). B cells: Secretory immunoglobulin A (sIgA). Dendritic cells: antigen sampling and presentation. Macrophages: pathogen clearance. Mast cells 6. Role of Secretory Immunoglobulin A (sIgA) Functions as a first-line defense in the intestinal mucus layer. Neutralizes pathogens, prevents epithelial adhesion. 7. Postbiotics Overview Bioactive compounds produced by gut microbiota. Examples: short-chain fatty acids (SCFAs) 8. Short-Chain Fatty Acids (SCFAs) and Their Functions Influence on Treg cells in the lamina propria, promoting immune tolerance. Butyrate also as an energy source for epithelial cells. 9. Supporting Butyrate Production Microbiome optimization to enhance beneficial butyrate-producing microbes. Use of prebiotics: resistant starch, soluble fibers, and polyphenols. Supplementation with sodium butyrate as an additional tool. 10. Other Postbiotics Antimicrobial peptides produced by beneficial microbes. Complex carbohydrates produced by beneficial microbes and can act as prebiotics. Polyphenol metabolites: Gut microbiota biotransforms polyphenols into bioactive metabolites with increased bioavailability. 11. Specific Polyphenols Examples: resveratrol, quercetin, and ellagitannins. Effects on intestinal barrier function, inflammation, and immune cell populations. "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Follow Chloe on TikTok @chloe_c_porter Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ --- Support this podcast: https://podcasters.spotify.com/pod/show/chloe-porter6/support

One of our MIB Agents OutSmarting Osteosarcoma 2024 grant recipients, Dr. Chris Richards, an Associate Professor from the University of Kentucky provides an overview of his funded work on macrophage engineered vesicles to treat pediatric osteosarcoma. This presentation focuses on the development of nanoscale vesicles derived from immune cells that can be utilized as immunomodulatory and therapeutic delivery platforms. Dr. Richards is a Professor in the Department of Chemistry at the University of Kentucky where he also serves as the Director of the Light Microscopy Facility and the Director of the Bioelectronics and Nanomedicine Center. His lab has developed novel nanoscale biomaterials for therapeutic delivery and in vivo sensing within the central nervous system. Incorporating these materials with nanofabricated devices has enabled his lab to develop new platforms for interrogating biological systems in cell culture, isolated tissue, and in vivo. Research in the Richards lab also focuses on the development of ensemble and single-molecule fluorescence spectroscopy techniques for the study of complex biological systems. His lab has recently applied this approach to study substance use disorders along with the development of therapeutic delivery platforms for cancer and spinal cord injury. Dr. Richards received his bachelor's degree in chemistry from the University of Maine and his PhD in physical chemistry from the Georgia Institute of Technology. He was also a postdoctoral researcher at Caltech where he was also a Beckman postdoctoral Scholar.

Immune explains how distinct olfactory mucosal macrophage populations mediate neuronal maintenance and pathogen defense, and failure to establish durable SARS-CoV-2-specific plasma cells in the bone marrow long-lived compartment after mRNA vaccination. Hosts: Vincent Racaniello, Cindy Leifer, Steph Langel, and Brianne Barker Subscribe (free): Apple Podcasts, RSS, email Become a patron of Immune! Links for this episode MicrobeTV Discord Server Nasal mucsosal macrophages, neuronal maintenance, and pathogen defense (Mucos Immunol) No long lived memory B cells after SARS-CoV-2 mRNA vaccination (Nat Comm) Time stamps by Jolene. Thanks! Music by Tatami. Immune logo image by Blausen Medical Send your immunology questions and comments to immune@microbe.tv

TWiV notes the passing of virologist Diane Griffin, first H5N1 influenza virus in US pigs, Innate immune control of influenza virus interspecies adaptation via IFITM3, and antiviral trained innate immunity in alveolar macrophages after SARS-CoV-2 infection reduces secondary influenza A virus disease. Hosts: Vincent Racaniello, Alan Dove, Rich Condit, Kathy Spindler, and Brianne Barker Subscribe (free): Apple Podcasts, RSS, email Become a patron of TWiV! Links for this episode MicrobeTV Discord Server MicrobeTV Fundraiser Diane Griffin passes (Johns Hopkins) Diane Griffin on TWiV 453 First H5N1 influenza virus in US pigs (CIDRAP) IFITM3 controls interspecies influenza virus infection (Nat Comm) Trained innate immunity by alveolar macrophages (Immunity) Timestamps by Jolene. Thanks! Weekly Picks Angela – See a giant ‘ghost particle' detector and more — October's best science images Brianne – October 27 APoD: Bat nebula Dickson – Nikon Small World Contest 2024 winners Kathy – AAAS 150th anniversary video, celebrating scientists and Pew's 2024 annual Trust in Science survey findings Rich – Cats Basically Are a Liquid After All, Study Confirms Alan – HHMI's Beautiful Biology site Vincent – EcoHealth Alliance Fights Back Listener Picks Hunter – Don't stop me now: Queen's Brian May on saving badgers — and the scientific method Anne – Reasons to be cheerful Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv Content in this podcast should not be construed as medical advice.

In this episode, we're joined by Noam Baumatz, CEO and Co-Founder of Noga Therapeutics, a company dedicated to developing gene therapies for rare and severe diseases through engineering macrophages. Motivated by his highly personal experience of rare disease, Noam founded Noga to develop the type of gene therapies his daughter was unable to access. He and Patrick discuss his work with parents and families affected by rare disease, the road to effective, financially accessible gene therapies, and Noam's previous work in traditional Chinese medicine.

On this episode of JHLT: The Podcast, the JHLT Digital Media Editors explore two studies from the July issue of The Journal of Heart and Lung Transplantation. Digital Media Editor Marty Tam, MD, a transplant cardiologist from the University of Michigan in Ann Arbor, hosts this episode.   First, Dr. Tam and Digital Media Editor Erika Lease, MD, FCCP, interview their first guest, Daniel Calabrese, MD, first author on the study “Macrophage and CD8 T cell discordance are associated with acute lung allograft dysfunction progression.” The study's authors sought to tackle challenges behind early detection of chronic lung allograft dysfunction (CLAD) by identifying biomarkers associated with acute lung allograft dysfunction (ALAD) progression to CLAD.   To do this, they collected bronchoalveolar lavage (BAL) cells at the time of ALAD diagnosis and performed single cell RNA sequencing to identify significant differences in 26 unique cell populations across groups, with discordant CD8 T cells and macrophages providing the best discrimination between ALAD with decline from ALAD with recovery and controls.   Dr. Calabrese discusses how his team identified the diagnostic criteria, why the biomarkers might lead ALAD to progress to CLAD, and how the findings might lead to early targeted therapies.   Next, Dr. Tam joins and Digital Media Editor Khue Ton, MD and David Schibilsky, MD, to interview their next guest, David D'Alessandro, MD, the Surgical Director of Cardiac Transplantation and MCS at Massachusetts General Hospital in Boston. Dr. D'Alessandro was the first author on the study “Impact of controlled hypothermic preservation on outcomes following heart transplantation,” which sought to assess the impact of the Paragonix SherpaPak Cardiac Transport System, a device allowing controlled hypothermic  preservation, on rates of primary graft dysfunction (PGD) and post-transplant mortality.   The key finding was that controlled hypothermic preservation was associated with a lower incidence of severe PGD – 6.6% compared to ice storage at 10.4%. In the conversation, Dr. D'Alessandro answers questions about the need for innovation over traditional ice cold storage, the greatest advantages of controlled hypothermic approaches, and the next steps in this research.   Follow along at www.jhltonline.org/current, or, if you're an ISHLT member, access your Journal membership at www.ishlt.org/jhlt.   Don't already get the Journal and want to read along? Join the International Society of Heart and Lung Transplantation at www.ishlt.org for a free subscription, or subscribe today at www.jhltonline.org.

Oxygen is activated quantum-mechanically in the body to act against bacterial infections. Professor Robert C Allen shows that the antibacterial action of oxygen can be monitored by measuring the light emitted as the immune system responds to pathogen attacks. He has developed techniques based on the use of chemiluminigenicmolecules which provide unprecedented insight into the neutrophil activity and afford powerful point of care diagnostic tools for immune system monitoring. Read more in Research Features: doi.org/10.26904/RF-151-6124846326Read the original research: doi.org/10.3390/antiox11030518

The key to understanding oxygen activation is the conversion of this molecule into a reactive singlet species within neutrophil cells in the blood. This process leads to light emission, which can be used to monitor in real time how the immune system functions.Based on over 40 years of research, Professor Robert C Allen proposes an exquisitely detailed model of how oxygen becomes an aggressive bactericidal agent in the body. Read more in Research Features: doi.org/10.26904/RF-151-6036339265Read the original research: www.intechopen.com/chapters/64123

Robert Towarnicki, CEO and Co-founder of SIRPant Immunotherapeutics, discusses cancer-specific immunotherapy for aggressive tumors, the role macrophages play in the immune response to cancer, and how cancer cells can shut down this response. SIRPant Immunotherapeutics aims to modify macrophages by reducing SIRPα expression, triggering them to eat cancer cells and educate other immune cells. Early evidence demonstrates potential effectiveness for various cancers, including non-Hodgkin's lymphoma and solid tumors. Robert emphasizes this therapy's scalability and cost advantages compared to other cell therapies like CAR-T. He also highlights the potential for treating rare diseases and the ability of SIRPant-M to target a wide range of cancers without the need for pre-identified targets. Robert explains, "Macrophages are a normal immune cell type in your body. They normally function to recognize foreign invaders and process them in the sense of phagocytizing or eating the foreign protein and invader, if it's a virus, a bacteria, or a cancer. Unfortunately, cancers are very good at shutting down this immune response. So, we need to modify the macrophage and re-empower it to elicit the other immune cells in the body to do their job and eliminate cancer." "I think one of the mistakes we've seen with others working with the macrophage in this situation was the lack of appreciation for the role of SIRPα. Our inventor, Dr. Yuan Liu at Georgia State University, identified this early on through a knockout mouse, a mouse where SIRPα was genetically removed from it. With that mouse, she could discover and learn how macrophages function and react. It directed us to the whole concept of removing SIRPα from the macrophage. Now, removal alone is not enough. You also have to activate a macrophage. So, a macrophage exists in multiple states. There's an active state, and then there's an inactive state." #SIRPant #Immunotherapy #Macrophages #Oncology #Cancer sirpantimmunotx.com Download the transcript here

Robert Towarnicki, CEO and Co-founder of SIRPant Immunotherapeutics, discusses cancer-specific immunotherapy for aggressive tumors, the role macrophages play in the immune response to cancer, and how cancer cells can shut down this response. SIRPant Immunotherapeutics aims to modify macrophages by reducing SIRPα expression, triggering them to eat cancer cells and educate other immune cells. Early evidence demonstrates potential effectiveness for various cancers, including non-Hodgkin's lymphoma and solid tumors. Robert emphasizes this therapy's scalability and cost advantages compared to other cell therapies like CAR-T. He also highlights the potential for treating rare diseases and the ability of SIRPant-M to target a wide range of cancers without the need for pre-identified targets. Robert explains, "Macrophages are a normal immune cell type in your body. They normally function to recognize foreign invaders and process them in the sense of phagocytizing or eating the foreign protein and invader, if it's a virus, a bacteria, or a cancer. Unfortunately, cancers are very good at shutting down this immune response. So, we need to modify the macrophage and re-empower it to elicit the other immune cells in the body to do their job and eliminate cancer." "I think one of the mistakes we've seen with others working with the macrophage in this situation was the lack of appreciation for the role of SIRPα. Our inventor, Dr. Yuan Liu at Georgia State University, identified this early on through a knockout mouse, a mouse where SIRPα was genetically removed from it. With that mouse, she could discover and learn how macrophages function and react. It directed us to the whole concept of removing SIRPα from the macrophage. Now, removal alone is not enough. You also have to activate a macrophage. So, a macrophage exists in multiple states. There's an active state, and then there's an inactive state." #SIRPant #Immunotherapy #Macrophages #Oncology #Cancer sirpantimmunotx.com  Listen to the podcast here

In this episode of The Metabolic Classroom, Dr. Ben Bikman challenges the traditional view that saturated fats are the primary cause of atherosclerotic plaques and heart disease. He asserts that while plaques, or atheromas, in coronary arteries are composed partly of fats and foam cells, the exact process of plaque formation remains speculative. Dr. Bikman emphasizes that anyone claiming to know the definitive cause of plaque formation is likely overstating their knowledge. Foam cells, which are fat-laden macrophages, play a critical role in plaque development and are consistently present at the sites of these plaques.Dr. Bikman explains that inflammation is a significant factor in atherosclerosis, and C-reactive protein (CRP), a marker of inflammation, is a better predictor of heart disease than LDL cholesterol. He describes how macrophages engulf oxidized LDL cholesterol, turning into foam cells and secreting pro-inflammatory proteins like CRP. This process is driven by the presence of oxidized lipids, particularly those derived from omega-6 polyunsaturated fats such as linoleic acid, which are prevalent in modern diets due to the widespread use of vegetable oils.Ben highlights several studies to support his argument. A notable study from 1979 by Brown and Goldstein showed that macrophages only consume LDL cholesterol when it is oxidized, not in its native form. Another study from 1998 found that oxidized LDL containing specific bioactive lipids, nine and 13 HODE, is particularly problematic. These oxidized lipids are derived from linoleic acid, not from saturated or monounsaturated fats. Moreover, historical dietary studies, such as the Minnesota Coronary Experiment and the Sydney Diet Heart Study, revealed that participants consuming more polyunsaturated fats had higher mortality rates than those consuming saturated fats.To conclude, Dr. Bikman argues that the traditional belief that saturated fat causes heart disease is flawed. He points out that recent studies, including a correlational study published in the British Medical Journal, show that refined grains, not saturated fats, are more strongly linked to heart disease and overall mortality. He suggests that the real dietary culprit is the overconsumption of omega-6 polyunsaturated fats, particularly linoleic acid, found in processed foods. This shift in perspective underscores the importance of reevaluating dietary guidelines and focusing on the types of fats consumed.#HeartHealth #SaturatedFat #Atherosclerosis #Inflammation #InsulinResistance #LDLCholesterol #OxidizedLDL #FoamCells #Macrophages #BenBikman #MetabolicHealth #CholesterolMyths #LinoleicAcid #PolyunsaturatedFats #DietaryFats #CardiovascularResearchStudies referenced:Binding Site on Macrophages that Mediates Uptake in Degradation by Brown and Goldstein (1979): https://academic.oup.com/clinchem/article/46/6/829/5641219 Oxidized LDL Regulates Macrophage Gene Expression (1998): You can find more details on this study in resources like ScienceDirect and Cell Journal (you may need specific access or subscriptions to retrieve full texts).Strong Increase in Hydroxy Fatty Acids Derived from Linoleic Acid in Human Low-Density Lipoproteins of Atherosclerotic Patients (1998): https://www.sciencegate.app/document/10.1016/s0009-3084(97)00095-9 Learn more: https://www.insuliniq.com Hosted on Acast. See acast.com/privacy for more information.

Episode #311. Some people follow a ketogenic diet seeking to lose weight, feel more energised, or gain control over their eating habits. Others may turn to this diet in an effort to treat their epilepsy, bipolar disorder, or diabetes. Regardless of their reasoning for adopting this eating pattern, a key question remains: can high LDL cholesterol levels on a ketogenic diet be safe? Today I sit down with Dr William Cromwell, MD and Dave Feldman to explore this question. In this discussion, Dr William Cromwell and Dave Feldman share their professional opinions on whether high cholesterol on a keto diet is a problem. We investigate where their opinions align and where they differ, where Dave's hypotheses diverge from the norm, and what we do and don't know with the available evidence. We also explore the significance of ApoB, lifespan and healthspan considerations, research Dave is currently conducting, and much more. Specifically, we discuss: Intro (00:00) Dr. William Cromwell: Background as a Lipidologist and LDL Research (01:54) Dave Feldman's Ketogenic Diet and Elevated LDL Experience (05:34) Unpacking the Lipid Hypothesis and Cardiovascular Risk (12:30) The history and evolution of the lipid hypothesis (20:40) The role of apoB lipoproteins in atherosclerosis (23:39) Factors beyond apoB involved in atherosclerosis and mortality risk (31:59) The complexity of interpreting mortality data in the context of apoB (41:40) Macrophages and the process of atherosclerosis (44:00) Beyond ApoB: Metabolic Vulnerability, Inflammation and Mortality Risk (52:57) Transcytosis: A New Perspective on LDL Movement and Atherosclerosis (1:10:36) Exploring Low Cholesterol Impacts and Genetic Disorders (1:17:30) Macrophage function and phenotype in the context of different drivers of high apoB (1:22:30) Defining Lean Mass Hyper-responders in the Context of a Ketogenic Diet (1:31:40) Investigating PCSK9 and Its Effects on Healthspan (1:38:00) Assessing cardiovascular risk in lean mass hyper-responders (1:43:50) Statin safety, adverse effects, and patient reluctance (2:01:54) Ketogenic Diets and Elevated LDL: Balancing Individual Risks and Benefits in the Absence of Long-term Data (2:10:40) Insulin Resistance, ApoB, and Cardiovascular Risk: Navigating the Challenges in Assessment and Imaging (2:18:12) Lean Mass Hyper-responder Study: Design, Recruitment, and Eligibility Criteria (2:32:45) Closing Perspectives on Research and Dietary Options (3:04:47) Outro (3:06:42) Connect with Dr William Cromwell on Twitter/X, LinkedIn, and his website, https://www.mylipid.com/. Discover more of his work with Precision Health Reports on Twitter/X, LinkedIn, Facebook, Instagram, and at https://precisionhealthreports.com/. Connect with Dave Feldman on Twitter/X, YouTube, and Instagram, and discover more of his work at https://citizensciencefoundation.org/, https://ownyourlabs.com/, and https://cholesterolcode.com/. This episode is brought to you by: InsideTracker If you want to improve your health, you need to measure where you're currently at. InsideTracker analyses up to 48 blood biomarkers including ApoB, LDL, HDL, A1C, and more before giving you advice to optimise your health. Get a 20% discount on your first order at insidetracker.com/simon. Shopify Shopify, the world's leading e-commerce platform, helps you turn browsers into buyers with the internet's best-converting check out–up to 36% better compared to other leading e-commerce platforms. To boost your conversion rate, and grow your business, sign up for a one-dollar-per-month trial period at shopify.com/proof. Sun Home Saunas Invest in your body and mind with Sun Home Saunas, pioneers in crafting premium saunas and cold plunges. Safe, effective, research-backed wellness tools to improve cardiovascular health, offer psychological benefits, and reduce muscle soreness. Head to sunhomesaunas.com/theproof for $300 off your purchase.

References Int J Mol Sci. 2019 Oct; 20(20): 5028. Lennon-McCartney. 1964. "Ill Be Back" https://youtu.be/fJSTBNTac6k?si=rr4rWE86TIs8EZcL Bruch, M. 1866. Violin Concerto 1. G minor https://youtu.be/9BeV9XDs64w?si=AvEAQch7T8TJrt05 --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support

TWiV reviews measles outbreaks in England and Europe, 2 fatal Nipah virus cases in Bangladesh, yellow fever outbreak in Sudan, and discuss how the type of immunodeficiency influences the outcome of SARS-CoV-2 infection, and programming of alveolar macrophages by intestinal bacteria that influences severity of respiratory viral infection. Hosts: Vincent Racaniello, Dickson Despommier, and Rich Condit Subscribe (free): Apple Podcasts, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode MicrobeTV Discord Server MicrobeTV store at Cafepress Become a member of ASV (asv.org) Research assistant position in Rosenfeld Lab CBER/FDA (pdf) The New City by Dickson Despommier Viruses of Microbes 2024 Pig virus imperils food security in Borneo (Science) Measles outbreaks in UK and Europe (Nature) Fatal Nipah virus infections in Bangladesh (CIDRAP) Yellow fever outbreak in Sudan (Crisis24) COVID-19 influenced by type of immunodeficiency (Sci Transl Med) Intestinal microbiota programming of alveolar macrophages (Cell Host Microbe) Letters read on TWiV 1085 Timestamps by Jolene. Thanks! Weekly Picks Dickson – JWST details of 19 spiral galactic centers Rich – Great White Shark Attack And Breach Vincent – Black History Month and Lost Photographs of Black America Listener Picks Louise – The Mystery Of The Village That Beat The Black Death Pierre – Three things airlines don't want you to know Brandon – Professor Dave explains Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv

Juliet Morrison joins Immune to discuss her career and the research of her laboratory showing that pleural macrophages translocate to the lung during infection to promote improved influenza outcomes. Hosts: Vincent Racaniello, Steph Langel, Cynthia Leifer, and Brianne Barker Guest: Juliet Morrison Click arrow to play Download Immune 76 (48 MB .mp3, 67 min) Subscribe (free): Apple Podcasts, Google Podcasts. RSS, email Become a patron of Immune! Links for this episode MicrobeTV Discord Server Publishing is broken (Solving for Science) Pleural macrophages move to the lung during influenza (PNAS) Time stamps by Jolene. Thanks! Music by Steve Neal Immune logo image by Blausen Medical Send your immunology questions and comments to immune@microbe.tv

Immune reveals the total mass (1.2kg), number (1.8 trillion), and distribution of immune cells in the human body, with macrophages contributing nearly 50% of the total cellular mass. Hosts: Vincent Racaniello, Cynthia Leifer, and Brianne Barker Subscribe (free): Apple Podcasts, Google Podcasts. RSS, email Become a patron of Immune! Links for this episode MicrobeTV Discord Server Immune cells in the human body (PNAS) Letters read on Immune 73 Time stamps by Jolene. Thanks! Music by Steve Neal. Immune logo image by Blausen Medical Send your immunology questions and comments to immune@microbe.tv

Immune explains how, in a mouse model of roundworm infection with Nippostrongylus brasiliensis, exposure to lung-migrating helminths protects mice against SARS-CoV-2 infection. Hosts: Cynthia Leifer, Stephanie Langel, and Brianne Barker Subscribe (free): Apple Podcasts, Google Podcasts. RSS, email Become a patron of Immune! Links for this episode MicrobeTV Discord Server Helminth protects against murine SARS-CoV-2 infection (Sci Immunol) Pandemic spared Africa (ScienceInsider) Letters read on Immune 71 Time stamps by Jolene. Thanks! Music by Steve Neal. Immune logo image by Blausen Medical Send your immunology questions and comments to immune@microbe.tv

A fascinating new look at treating periodontal disease using macrophages differently. Katrina Sanders, RDH takes a look at work coming from Kings College in London related to using telocytes as a regulator of M1 vs M2 macrophages! Resources: More Fast Facts: https://www.ataleoftwohygienists.com/fast-facts/ Katrina Sanders Website: https://www.katrinasanders.com  Katrina Sanders Instagram:   https://www.instagram.com/thedentalwinegenist/  Jing Zhao, Anahid A Birjandi, Mohi Ahmed, Yushi Redhead, Jose Villagomez Olea, Paul Sharpe (2022). Telocytes regulate macrophages in periodontal disease. Published in eLife https://doi.org/10.7554/eLife.72128