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Immune System

Episodes

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Q&A #64 with Dr. Rhonda Patrick (11/2/24)

Posted on November 19th 2024 (7 months)

Dr. Rhonda Patrick discusses silicone safety, grounding, pentadecanoic acid, and the potential benefits of olive leaf extract and peptides.

sleep

How Heat Therapy Improves Slow Wave Sleep

Posted on May 30th 2023 (about 2 years)

Heat therapy (saunas, exercise, hot baths) can enhance slow-wave sleep. This video explores exercise and heat's joint role in sleep regulation.

ketogenic diet

The ketogenic diet and cancer research | Dominic D'Agostino

Posted on May 21st 2022 (about 3 years)

In this clip, Dr. Dominic D'Agostino discusses the implications of adding a ketogenic diet to cancer treatment protocols.

Topic Pages

  • Blood-brain barrier

    Blood-brain barrier regulates CNS immune surveillance by limiting leukocyte transmigration and selectively transporting cytokines and antibodies.

  • Breast milk and breastfeeding

    Breast milk delivers maternal antibodies, immune cells, and cytokines that passively protect infants and shape neonatal immune maturation.

  • Butyrate

    Microbiota-derived butyrate modulates immune homeostasis by HDAC inhibition, enhancing colonic regulatory T-cell differentiation and anti-inflammatory cytokine production.

  • Cold exposure

    Cold exposure stimulates sympathetic-adrenal catecholamine release and brown-adipose thermogenesis, collectively altering leukocyte trafficking and proinflammatory cytokine profiles.

  • Omega-3 fatty acids

    Omega-3 PUFA-derived resolvins and maresins suppress pro-inflammatory cytokine production, thereby modulating innate and adaptive immune responses.

  • Thymic involution

    Age-associated thymic involution diminishes thymopoiesis, thereby reducing naïve T-cell repertoire and weakening systemic adaptive immunity.

  • Toll-like receptors

    Toll-like receptors initiate innate immune signaling by recognizing pathogen-associated molecular patterns and activating downstream NF-κB-mediated cytokine production.

News & Publications

  • Regular blood donation promotes beneficial stem cell mutations while minimizing disease risk by inducing genetic changes that preferentially support healthy red blood cell production. ashpublications.org
    Cancer Stem Cells Immune System Genetics

    Donating blood is an act of generosity that saves lives, yet few donors think about how it affects their own health. Each donation triggers a surge in blood cell production, a process that could subtly shape the long-term health of blood-forming stem cells. A recent study found that frequent blood donation promotes the expansion of specific blood stem cell mutations that support healthy red blood cell production.

    Researchers analyzed blood samples from 217 older men who had donated more than 100 times and compared them to 212 men who had donated fewer than 10 times. They looked for clonal hematopoiesis, a condition where blood stem cells acquire genetic changes that allow specific cell populations to expand. They also used gene-editing techniques to study how particular mutations behaved when exposed to erythropoietin, a hormone that increases after blood loss.

    They found that the overall rate of clonal hematopoiesis was similar between frequent and infrequent donors. However, mutations in the DNMT3A gene showed distinct patterns in frequent donors. Some of these mutations responded to erythropoietin by expanding, while others, known to be associated with leukemia, were more likely to grow in response to interferon-gamma, a protein involved in the immune response. Further analysis revealed that the erythropoietin-responsive mutations tended to push blood stem cells toward making more red blood cells rather than leading to abnormal or harmful changes.

    These findings suggest that repeated blood donation encourages the expansion of specific blood stem cell mutations, but the effects support normal blood cell production rather than increase disease risk. Blood donation also lowers levels of iron—a key nutrient that, in excess, harms the brain. Learn more in this episode featuring Dr. Gordon Lithgow.

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  • Food antigens, proteins in meat and milk that trigger allergic reactions, activate immune responses that reduce the risk of small intestinal tumors. www.frontiersin.org
    Cancer Diet Immune System Allergies Protein

    Proteins in milk, meat, and other foods can trigger allergic reactions in some people. However, these proteins—called antigens—can also interact with the immune system to suppress small intestinal tumors. A recent study in mice found that food antigens help activate immune responses in the small intestine, potentially reducing the risk of tumors.

    Researchers fed mice genetically prone to developing intestinal tumors—similar to the genetic predisposition to familial adenomatous polyposis in humans—an antigen-free diet to pinpoint the role of food components in immune activation. They also depleted immune tissues in the animals' small intestines called Peyer’s patches to investigate how food antigens trigger immune cells.

    They found that food antigens activate immune cells in Peyer’s patches, suppressing small intestinal tumor formation. This immune response is crucial for maintaining a tumor-suppressive environment in the gut.

    These findings suggest that food antigens help protect against small intestinal tumors in mice by activating immune cells that promote tumor suppression, highlighting their potential as a protective factor in gut health. The microbiome plays a key role in gut health, too. Learn more in this episode featuring Dr. Eran Elinav.

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  • People with tattoos have a 21% increased risk of malignant lymphoma, with laser tattoo removal further amplifying the risk to 163%. www.thelancet.com
    Cancer Immune System

    Body art is more popular than ever, with roughly one-third of people in the U.S. having at least one tattoo. However, tattoo inks often contain harmful chemicals, including carcinogenic pigments and metals. A recent study found that people with tattoos are 21% more likely to develop malignant lymphoma.

    Researchers conducted a case-control study among roughly 1,400 people diagnosed with malignant lymphoma (“cases”) in people aged 20 to 60 over 10 years. They matched the cases with age- and sex-matched people without cancer (“controls”) from the general population. Then, they gathered information about the participants' tattoo exposure and assessed the relationship between tattoos and lymphoma risk.

    They found that overall, participants with tattoos were 21% more likely to develop malignant lymphoma than those without. The risk of lymphoma among those who had received their first tattoo within the previous two years was 81% higher than those without a tattoo. Risk decreased nearly to baseline between three and 10 years after the first tattoo but increased again to 19% after 11 years, suggesting that long-term exposure to tattoo-related chemicals contributes to a delayed but persistent risk of developing lymphoma.

    Undergoing laser removal of tattoos increased the risk of lymphoma by 163%. Oddly, greater tattoo surface area did not increase risk, with the highest lymphoma risk among people with tattoos smaller than the size of a deck of cards.

    These findings point to potential links between tattoos and an increased risk of lymphoma. The tattooing process involves injecting ink into the skin through repeated punctures, breaching the skin’s protective barrier and triggering an immune response. As the ink enters the body, immune cells called macrophages attempt to engulf and isolate the foreign substance, driving the movement of pigment to nearby lymph nodes. Lasering tattoo ink induces the formation of toxic, carcinogenic substances that can persist in the body.

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  • Ovarian cancer tumors, even at advanced stages, may be effectively targeted and eliminated by CAR-T immune therapies, a new study in mice suggests. www.sciencedaily.com
    Cancer Genetic Engineering Immune System

    CAR-T, or chimeric antigen receptor T-cell therapy, is an immunotherapy approach that involves genetically modifying a person’s own T cells so they can recognize and target specific proteins on cancer cell surfaces, enhancing the immune system’s capacity to seek out and destroy malignant cells. CAR-T therapies have been successful against blood cancers, such as leukemia, lymphoma, or myeloma, but have largely failed with solid tumors. Now, a new study in mice demonstrates that CAR-T is effective against ovarian cancer, nearly doubling survival time.

    Researchers identified a unique carbohydrate present only on the surface of solid tumor cells, not healthy ones, and engineered CARs with a strong affinity for the carbohydrate. Then, they delivered the CAR-T therapy via intravenous injection to mice with ovarian cancer. Because ovarian cancer treatments delivered directly into the abdominal area are particularly effective, they also administered the CAR-T therapy into the animals' abdomens.

    They found that the CAR-equipped T cells effectively located and eliminated the cancer cells, promoting tumor shrinkage or elimination with just one dose. The genetically engineered cells maintained their effectiveness for several months, with no evidence of toxicity or adverse effects. Intravenous injection of CAR-T cells increased survival to 145 days, but direct delivery into the animals' abdomens extended survival to 270 days.

    These findings demonstrate that modified CAR-T cells show promise as a potential treatment for ovarian cancer and other solid tumors. Future studies are needed to assess the treatment’s effectiveness in humans. Learn more about genetic engineering in this episode featuring Dr. George Church.

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  • Swabbing C-section newborns with their mothers' vaginal fluid promotes healthier neurodevelopment at 3 and 6 months, bridging the gap to vaginally del www.newscientist.com
    Microbiome Immune System Pregnancy Development

    Infants born by cesarean section have different microbial communities in and on their bodies than those born vaginally, potentially increasing their risk of developing certain diseases, such as asthma and obesity. But a new study shows that vaginal microbiota transfer – exposing newborns to fluids from their mother’s vagina – may rectify these differences.

    The study involved 68 infants born by cesarean section. Researchers swabbed the infants' skin with sterile gauze soaked in either the mother’s vaginal fluids or saline immediately after birth. They assessed the infants' neurodevelopment at three and six months of age and analyzed the microbial makeup of the infants' guts.

    They found that infants who received vaginal microbiota transfer scored higher on neurodevelopment assessments than those who received saline. They also had healthier, more mature gut microbiomes – comparable to infants born vaginally.

    These findings suggest that exposing infants born via cesarean section to their mother’s vaginal fluids promotes appropriate neurodevelopment and corrects alterations in gut microbial populations. Learn more about the importance of establishing a healthy microbiome early in life in this clip featuring Dr. Eran Elinav.

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  • Blocking the body's antiviral immune response holds promise for Alzheimer's disease prevention. medicalxpress.com
    Alzheimer's Aging Immune System Virus

    The immune system plays important, and sometimes surprising, roles in brain health. A new study in mice found that blocking components of the antiviral immune response may make the brain more resilient to the effects of abnormal tau – potentially preventing Alzheimer’s disease and other forms of dementia.

    Tau is a protein found in the brain. Abnormal tau can form aggregates called tau tangles – one of the defining characteristics of Alzheimer’s disease – activating antiviral response pathways and interfering with normal brain function and cognition.

    Researchers studied the effects of exposure to abnormal tau on microglia, the brain’s resident immune cells. They found that when microglia were exposed to abnormal tau, the mitochondria became “leaky,” releasing their DNA into the cellular fluid. The immune system inappropriately interpreted the leaked DNA as a viral attack, triggering an immune response that promoted the release of type-I interferon, a cytokine that drives the antiviral immune response. Interrupting the pathways involved in this response restored normal brain function.

    These findings suggest that suppressing the inappropriate immune response to abnormal tau exposure could provide a means to prevent or treat the tau-associated pathologies common in Alzheimer’s disease and dementia. Learn about other strategies to reduce the risk of Alzheimer’s disease in this episode featuring Dr. Dale Bredesen.

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  • Obese when compared to those with normal body fat had much higher inflammation: 53% higher CRP, 30% higher TNF-a, 17% higher WBC count, 42% higher IL6 linkinghub.elsevier.com
    Obesity Aging Metabolism Inflammation Immune System Metabolic Syndrome IL-6

    Strong link between accumulated visceral fat and chronic inflammation.

    A person’s waist-to-hip ratio compares their waist measurement to that of their hips. A high ratio can be an indicator of excess fat accumulation around the waist, often referred to as visceral fat. Findings from a 2005 study suggest that visceral fat is associated with markers of inflammation.

    Visceral fat is stored in the abdominal cavity near the liver, pancreas, and intestines. The accumulation of visceral fat is linked to increased risk of cardiovascular disease and other chronic diseases. Many factors drive visceral fat accumulation, including poor sleep, an obesogenic diet, and sugar-sweetened beverage intake, among others.

    The study involved more than 3,000 healthy males and females (18 to 89 years old) living in Greece. The investigators calculated the participants' body mass index (BMI) and measured their waist and hip circumferences. Participants provided blood samples for the assessment of inflammatory biomarkers, including C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), amyloid A (an apolipoprotein secreted in the acute stage of inflammation), white blood cells, and interleukin-6 (IL-6).

    The investigators found that approximately 36 percent of the males and 43 percent of the females had excess visceral fat. Approximately 20 percent of the males and 15 percent of the females had obesity. Participants with greater visceral fat had 53 percent higher CRP, 30 percent higher TNF-alpha), 26 percent amyloid A, 17 percent higher white blood cell counts, and 42 percent higher IL-6, compared to participants with normal fat distribution. The relationship between visceral fat and inflammatory markers was stronger than that between obesity and inflammation, even when considering the participants' age, income, education, and other potential confounding factors.

    These findings suggest that visceral fat and inflammatory processes are linked. The investigators posited that excess accumulation of visceral fat may increase the risk for cardiovascular disease by driving inflammation.

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  • Curcumin may act as an intervention in chronic urinary tract infection through dampening of toll-like receptors and reducing bacterial colony count pubmed.ncbi.nlm.nih.gov
    Microbiome Immune System Curcumin Microbes Toll-Like Receptors

    Curcumin reduces urinary tract infection symptoms via interaction with toll-like receptors.

    Urinary tract infections are common outpatient infections. They occur more frequently among women, and 50 to 60 percent of all women report having had at least one UTI in their lifetime. Findings from a 2017 study suggest that curcumin reduces the symptoms associated with urinary tract infections via interaction with toll-like receptors.

    Toll-like receptors comprise a family of pattern recognition receptors expressed on the surfaces of immune and other cells. They are the principal inducers of innate immunity and are responsible for the activation of transcription factors that increase the expression of proinflammatory cytokines. Chronic infections of the urinary tract, which either don’t respond to treatment or keep recurring, can occur in some people.

    Curcumin is a bioactive compound found in the roots of Curcuma longa, a type of tropical plant. It is responsible for the vibrant yellow color of the spice turmeric. Evidence suggests that curcumin exerts robust antioxidant, anti-inflammatory, and anticancer effects. Curcumin also exhibits antibacterial activity, but the compound is strain-specific.

    The study involved rats that had chronic urinary tract infections. Half of the rats received a curcumin injection, while the other half did not. The investigators measured the animals' white blood cell counts, bacterial counts (in the bladder and urine), markers of inflammation, and expression of toll-like receptor (TLR)2 and TLR4.

    They found that white blood cell counts, bacterial counts, markers of inflammation, and expression of TLR2 and TLR4 of the rats that received the curcumin injection were considerably lower than those of the rats that didn’t receive curcumin. These findings suggest that curcumin improves the symptoms of chronic urinary tract infections and reduces inflammatory responses via dampening the expression of TLR2 and TLR4.

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  • New research identifies critical differences between the two types of vitamin D, with vitamin D2 having a questionable impact on human health. www.sciencedaily.com
    Vitamin D Immune System Autoimmunity

    Vitamins D2 and D3 exert differing effects on the human immune system.

    Scientists have identified five forms of vitamin D, but the two primary forms relevant to human health are ergocalciferol, commonly referred to as vitamin D2 (produced by invertebrates), and cholecalciferol (produced by mammals), commonly referred to as vitamin D3. Prescription vitamin D supplements in the United States typically provide D2, but over-the-counter dietary supplements and fortified foods typically provide D3. Considerable controversy exists regarding the bioequivalence of D2 and D3. Findings from a recent study suggest that D2 and D3 exert differing effects on the human immune system.

    Vitamin D modulates both innate and adaptive immune responses via its interactions with immune cells, including antigen presenting cells, B cells, and T cells. Evidence suggests that people with vitamin D deficiency are at greater risk of viral infection and autoimmune disorders. This is in keeping with the widely held belief that a principal role of vitamin D is to restrain, or balance, immune system activity.

    The study was part of a previous randomized placebo-controlled trial involving healthy white European and South Asian females who received 15 micrograms (600 IU) of vitamin D2 or D3 every day for 12 weeks during the winter months, when sun exposure was limited. Participants also consumed vitamin D-fortified foods (orange juice and tea biscuits) daily. The investigators used microarray analysis to measure changes in 97 of the participants' blood transcriptome (the full range of RNA molecules an organism produces) and weighed the changes against any influence of ethnic background.

    They found that while the effects of both D2 and D3 showed some overlap, the two forms of the vitamin showed distinct differences in terms of changes to gene expression. In particular, D3 switched off the activity of genes involved in the regulation of the innate and adaptive immune systems. The investigators posited that these changes could make the immune system more tolerant and therefore less likely to promote autoimmunity. They also noted that vitamin D3 (and not D2) had a dramatic effect on genes involved in activation of interferon, which plays important roles in providing protection against pathogens and cancer. The investigators' analysis revealed that some of the variation in overall gene expression was likely due to ethnic differences among the participants.

    These findings suggest that vitamins D2 and D3 exert differing effects on the human immune system, with D3s effects modulating tolerance and immunoreactivity. They also may have relevant implications for supplementation with vitamin D.

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  • Mechanical forces of pressure and movement from exercise increases the formation of bone and lymphocytes, enhancing the ability to clear infection www.sciencedaily.com
    Exercise Aging Immune System Bone

    From the article:

    Researchers from the Morrison laboratory discovered that forces created from walking or running are transmitted from bone surfaces along arteriolar blood vessels into the marrow inside bones. Bone-forming cells that line the outside of the arterioles sense these forces and are induced to proliferate. This not only allows the formation of new bone cells, which helps to thicken bones, but the bone-forming cells also secrete a growth factor that increases the frequency of cells that form lymphocytes around the arterioles. Lymphocytes are the B and T cells that allow the immune system to fight infections.

    When the ability of the bone-forming cells to sense pressure caused by movement, also known as mechanical forces, was inactivated, it reduced the formation of new bone cells and lymphocytes, causing bones to become thinner and reducing the ability of mice to clear a bacterial infection.

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  • Brain’s own immune cells "infect" healthy neurons with Alzheimer-linked beta-amyloid protein. www.nature.com
    Alzheimer's Immune System

    Alzheimer’s disease is a common neurodegenerative disorder affecting an estimated 24 million older adults worldwide. Researchers believe the disease is caused by toxic levels of beta-amyloid protein aggregates in the brain that impair neuronal function and trigger cognitive decline. While this process is partly under the influence of genes, studies also indicate links between Alzheimer’s and external factors such as head injury. Findings from a new study shed new light on this link, suggesting that events such as head trauma and stroke accelerate Alzheimer’s disease by activating one of the brain’s major immune cells and triggering an infection-like spread of amyloid-beta tangles to previously unaffected tissues.

    The researchers conducted their experiments in mice genetically engineered to carry five mutations associated with Alzheimer’s disease. While these mutations lead to brain beta-amyloid aggregations and cognitive impairments at an early age, the team uncovered that even genetically healthy brain tissue could accumulate these aggregations if implanted into the brains of these mutant mice.

    To better understand this infection-like phenomenon, the researchers examined whether the mutant brain cells of the host might import beta-amyloid particles by migrating into the transplanted tissue or making connections with its neurons. Tracking them under a microscope offered no support for this hypothesis. Instead, the team uncovered a mass migration into the implanted tissue of microglia, the main immune cells of the nervous system, specialized for scouting brain tissue for signs of injury or pathogen invasion and clearing out cellular debris.

    One possible reason for this migration is that microglia are drawn to wounds. Indeed, the microglia were particularly concentrated around the edges of the transplant and exhibited similar migrations to tiny brain lesions that the researchers generated using lasers. However, in moving from the genetically diseased to healthy tissue, the microglia dumped large numbers of beta-amyloid particles previously picked up from the degenerating host brain tissue.

    The results offer an updated picture of Alzheimer’s disease progression where the brain’s own immune cells inadvertently drive the spread of pathogenic beta-amyloid aggregations – an effect that might be aggravated by brain injury events and inflammation. While scientists are uncertain why contaminated microglia engage in this “dumping” practice, targeting the cells' activity as a way of interfering with the neurodegenerative process provides promising research opportunities.

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  • The brain can remember and resurrect immune responses to previous infections. www.scientificamerican.com
    Brain Immune System

    The brain’s inner workings have traditionally been viewed as separate from “unconscious” physiological functions like immunity. Yet, recent research has uncovered a surprising degree of reciprocal brain-immune system interaction. For example, biomarkers of peripheral immunity influence brain aging and cognition, and dopamine-rich reward circuits in the brain influence systemic antibacterial activity in immune cells. A recent study now reveals that specific brain cells store memories of the body’s past experiences with infections, potentially reawakening previous immune responses.

    The researchers first measured brain activity in a group of mice that had inflammatory bowel disease. Their measurements revealed that the bowel inflammation and its associated immune response generated a broad pattern of activity across several regions of the brain, especially the insular cortex, a region considered crucial for receiving and processing information about internal bodily states and immune system activities.

    Then, to test whether the pattern of neuronal activity in the insular cortex represented a true memory of bowel inflammation, they examined how the mice reacted when the insular neurons were reactivated four weeks after the animals' recovery from illness. The result was a near-perfect revival of the original immune response to bowel inflammation, including a surge of white blood cells to the colon, heightened activation of a range of T-cells specialized for sensing and attacking pathogens, and a spike in pro-inflammatory molecules such as interleukins and tumor necrosis factor-alpha.

    The brain-induced immune event exhibited two features that indicated it was a form of recollection. First, it was exclusively located in the colon, suggesting a relatively precise “memory” of bowel inflammation rather than a generic signal for immune defense. Second, a repeated experience with simulated bowel disease caused the insular cortex to generate a new and largely non-overlapping pattern of immune-triggering activity. This indicates that the insular cortex is capable of “remembering” distinct episodes of the body’s encounters with disease.

    This study provides some of the first causal evidence that brain cells can form memories of past immune reactions – a property that may have evolved to help bodily tissues become faster and more precise in how they tackle future infections. While the mechanisms of these neuro-immune interactions are not fully understood, the interactions offer the potential for targeted insular brain stimulation to treat severe autoimmune and inflammatory health conditions.

    Link to full publication.

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  • Eating spices reduces chronic inflammation. academic.oup.com
    Inflammation Immune System Polyphenol Lipopolysaccharide

    Obesity causes chronic inflammation, which promotes atherosclerosis and cardiovascular disease. Previous research suggests that spices such as cinnamon, cumin, and ginger exert short-term anti-inflammatory effects; however, studies with longer durations are needed to confirm these findings. Authors of a recent study found that four weeks of spice consumption reduced inflammation and altered monocyte function in adults at risk of cardiometabolic disease.

    Monocytes are white blood cells that respond to infection by promoting inflammation. Obesity and dyslipidemia cause inappropriate activation of monocytes, promoting chronic inflammation in the arteries. Pro-inflammatory monocytes carrying excess lipids, called foam cells, accumulate in arterial walls, narrowing the arteries and restricting blood flow. Consuming spices that contain anti-inflammatory bioactive compounds may help reduce cardiovascular disease risk.

    The authors recruited 71 participants and assigned them to consume a standard American diet with added spices in three doses: low (a dash), medium (a quarter teaspoon), or high (a half teaspoon). Participants consumed each dose of spices for four weeks and completed the doses in random order. The spice mixture contained the most common spices used in the United States, the most abundant of which were cinnamon, coriander, ginger, cumin, and parsley. Participants provided blood samples at multiple points throughout the study. Finally, the investigators isolated monocytes from the participants’ blood and exposed the cells to bacterial endotoxin in order to promote inflammation.

    Compared to baseline, participants had lower fasting serum levels of the pro-inflammatory cytokine interleukin-6 following four weeks of the medium dose spice blend. The monocytes from these participants also secreted less interleukin-6 when challenged with bacterial endotoxin. Participants consuming the medium and high spice blends had fewer foam cells and more conventional monocytes than participants consuming the low spice blend.

    The authors concluded that spices reduced fasting inflammation and altered monocyte behavior. They did not know why the medium dose was more effective in reducing inflammation than the high dose, but they hypothesized that the high dose of spices may have contained such a high level of polyphenols that it promoted oxidative stress. More research is needed to test this hypothesis. This study was funded by the McCormick Science Institute.

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  • mRNA vaccines provide long-lasting immunity and protection from SARS-CoV-2 variants. www.bloomberg.com
    Immune System Vaccine COVID-19

    SARS-CoV-2 mRNA vaccines (e.g., Moderna and Pfizer-N-BioTech) are effective in preventing infection and have even greater efficacy in preventing severe COVID-19 illness and hospitalization. However, many people in the United States received their vaccine early in 2021, more than six months before the time of this writing. Whether the protection afforded by vaccination lasts as time passes and more SARS-CoV-2 variants emerge is unclear. Findings of a report published in August provide insights into long-term immunity following vaccination or SARS-CoV-2 infection, concerns about emerging variants, and implications for vaccination boosters.

    During infection with a virus, the innate immune system immediately produces inflammation to fight the infection. Within days or weeks, the adaptive immune system produces antibodies that are specific to the virus. These antibodies bind to a small piece of the viral particle, called an antigen. White blood cells such as macrophages and neutrophils participate in the innate response, while B and T cells facilitate the adaptive response. Plasma B cells are responsible for producing antibodies; however, these cells steadily decrease in number over time. Memory B cells store the genetic information needed to produce virus-specific antibodies upon reinfection. Memory T cells are also responsible for “remembering” viruses in this way. Memory CD4+ T cells rapidly respond to reinfection to support inflammation and antibody production. Memory CD8+ T cells, also called cytotoxic T cells, bind to virus-infected host cells and order them to undergo apoptosis (i.e., programmed cell death).

    The authors of the report analyzed a set of 342 blood samples collected from 61 participants at one, three, and six months following vaccination. This group of participants included SARS-CoV-2 naive individuals (i.e., those who were never infected with the virus) and SARS-CoV-2 recovered individuals. The investigators measured the concentration of circulating antibodies that bind to the SARS-CoV-2 receptor binding domain protein and spike protein. They also measured the concentration of memory B cells and T cells and characterized these cells’ response when challenged with SARS-CoV-2 antigens.

    The concentration of serum antibodies declined over time, but was still detectable at six months post-vaccination. mRNA vaccination produced memory B cells that respond to the receptor binding domain protein of the Alpha, Beta, and Delta variants, called cross-binding memory. These memory B cells had significantly more hypermutation, the process by which B cells rearrange their DNA in order to produce antibodies to new antigens, and increased in concentration between three and six months post-vaccination. Cross-binding B cells were more common in SARS-CoV-2 recovered patients than naive patients. mRNA vaccination also increased memory CD4+ and CD8+ T cells.

    The immune response to mRNA vaccination and infection with the SARS-CoV-2 virus evolves over time, which may have implications for the future use of booster vaccines. These results should be considered with caution as this research has yet to be peer-reviewed.

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  • Fecal microbiota transplantation from young mice reverses aging effects. www.sciencedaily.com
    Brain Aging Microbiome Immune System Microbes

    Declines in brain function are common with age owing to metabolic and immune alterations that include changes to the gut microbiota, the community of microorganisms that inhabit the intestines. While a diverse microbial community with many species of beneficial bacteria is associated with improved nutrition and reduced inflammation, older adults (especially residents of long-term care facilities) have perturbations in microbiota composition that increase the risk for cognitive decline and frailty. Findings of a report released this month show that fecal microbiota transplantation from young to aged mice reverses age-associated cognitive impairment.

    Fecal microbiota transplantation is a therapy in which microbes are isolated from the stool of a donor, processed, filtered, and administered to a recipient by nasogastric tube or enema. Previous research demonstrates the efficacy of fecal microbiota transplantation in treating infection with Clostridium difficile, a hospital-acquired infection that is difficult to treat with antibiotics, and a growing list of other diseases such as inflammatory bowel disease, metabolic syndrome, neurodevelopmental disorders (e.g., autism), and autoimmune diseases. Fecal microbiota transplantation improves health partially by increasing microbiota alpha diversity, meaning the number of species in an individual’s microbiota, also called “richess.” A microbiota with high richness is more likely to contain key beneficial species, such as those that produce neuroprotective short chain fatty acids.

    Given the wide range of diseases associated with gastrointestinal microbiota composition, its effects on aging are an area of intense interest. Prior investigations have demonstrated that transfer of the fecal microbiota from aged mice to young mice alters immunity, neurogenesis, and cognition; however, the consequence of fecal transplantation from young mice to aged mice is unknown.

    The investigators performed their experiment using young and aged male mice. They assigned aged mice to receive a fecal microbiota transplant from either a young mouse (the experimental group) or aged mouse (the control group). For further comparison, the researchers also assigned a group of young mice to receive a fecal microbiota transplant from another young mouse. Mice received the fecal microbiota transplant treatments once per day for three days, then twice weekly for four weeks. The mice completed a battery of tests to assess cognitive function. The researchers collected fecal samples in order to sequence the DNA of the microbiota and blood samples in order to measure hormones, cytokines, and other immune markers before and after the four weeks of treatment. Finally, they analyzed changes to gene expression and metabolism in the hippocampus, the brain region most-associated with age-related cognitive decline.

    At baseline, young and aged mice had distinctly different microbiota composition. Following four weeks of microbiota transplantation, young mice, aged mice receiving a young transplant, and aged mice receiving an aged transplant all had similar microbiota composition. Aged mice tended to have more over-reactive T cells, dendritic cells, and macrophages, especially in the lymph nodes that line the intestines. Aged mice also showed enlargement of microglia (the predominant immune cells in the brain), a common feature of neurodegenerative diseases. Microbiota transplantation from young mice reversed these age-related effects on brain and peripheral immunity. Amino acid metabolism in the hippocampus, which is necessary for neurotransmission and cognition, was impaired in aged mice, but restored following microbiota transplantation from young mice. Finally, the improved hippocampal metabolism in aged mice that received a young microbiota transplant translated to increased learning and long-term memory and reduced anxiety-related behaviors compared to aged mice receiving an aged microbiota transplant.

    These results reveal the potential benefits of fecal microbiota transplantation from young donors as a therapy to promote healthy aging.

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  • Large doses of vitamin C up to 8 grams per day might reduce duration of common cold. www.sciencedaily.com
    Vitamin C Immune System

    The bulk of scientific research on the effectiveness of vitamin C in fighting infection has centered on reducing the symptoms and duration of the common cold. Much of the studies have used doses of approximately 1 gram per day. Findings from a 2017 study suggest that larger doses might reduce a cold’s duration.

    Although most adults typically have only one or two colds per year, cold symptoms are the reason for many lost days of work or school. Some evidence suggests that the financial costs associated with having a cold are similar to those associated with having high blood pressure or a stroke.

    The author of the study reviewed the findings of two randomized trials focused on the effectiveness of vitamin C in reducing cold symptom duration. One of the trials had four treatment groups: one group that took a placebo, two groups that took 3 grams per day, and one group that took 6 grams per day. The 6-gram dose reduced cold symptom duration by about 17 percent – roughly twice as much as that observed with only 3 grams. The placebo had no effect on symptom duration. The other trial had three treatment groups: one that took 4 grams per day, one that took 8 grams per day, and one that took a placebo. Taking 8 grams per day reduced symptom duration by 21 percent, compared to the placebo group.

    These findings suggest that large doses of oral vitamin C might reduce the duration of symptoms associated with the common cold, but self-dosing should commence as soon as cold symptoms appear for the greatest benefit.

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  • Early life bacterial exposures influence immune health. www.the-scientist.com
    Immune System Salt

    The skin microbiota forms the body’s first line of defense against pathogens and external threats. Changes in environmental exposures can drive bacterial dysbiosis, a condition in which the overall makeup of the skin microbiota is altered. Bacterial dysbiosis is associated with allergies and sensitivities. A new study suggests that exposure to Acinetobacter bacteria early in life provides protection against inflammatory disorders and allergies. Acinetobacter bacteria are ubiquitous in the environment and are commonly found in soil.

    The study was conducted among 180 children living in Karelia, a region that straddles the geopolitical borders of Finland and Russia. Whereas the Finnish side of Karelia is modernized, the Russian side has maintained a traditional lifestyle that involves farming and animal work. The children from the two regions were examined for symptoms of allergies and sensitivities to common allergens when they were between the ages of 7 and 11 years and again when they were between the ages of 15 and 20 years. Samples of the children’s skin and nasal microbiota were collected for analysis.

    The prevalence of allergies and allergen sensitivities was 3 to 10-fold higher among Finnish children, compared to Russian children. In addition, Russian children rarely exhibited hay fever or peanut sensitivity. Generally, these findings were replicated at the 10-year follow-up examination. The children’s skin and nasal microbiota demonstrated notable differences. In particular, the Russian children’s microbiota had a diverse, abundant population of Acinetobacter bacteria. These findings suggest that early life exposures modulate the risk of developing allergies and allergen sensitivities later in life.

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