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Keto Diet May Ease Multiple Sclerosis Symptoms - Neuroscience News
New research suggests the ketogenic diet could help manage multiple sclerosis (MS) by promoting the production of beneficial compounds in the gut. In a study, mice on a keto diet produced the ketone body β-hydroxybutyrate (βHB), which worked with gut bacteria to create immune-modulating metabolites. This interaction reduced inflammation and improved MS symptoms in mice.
'Revelatory' study finds a smoking impact that remains after quitting
People who smoked had increased inflammatory responses, but those higher levels were transient, dropping after smoking cessation. But the effects on the adaptive response persisted for many years after quitting, changing the levels of cytokines released after infection or other immune challenges.
“Inverse vaccine” shows potential to treat multiple sclerosis and other autoimmune diseases | Pritzker School of Molecular Engineering | The University of Chicago
The inverse vaccine, described in Nature Biomedical Engineering, takes advantage of how the liver naturally marks molecules from broken-down cells with “do not attack” flags to prevent autoimmune reactions to cells that die by natural processes. PME researchers coupled an antigen — a molecule being attacked by the immune system— with a molecule resembling a fragment of an aged cell that the liver would recognize as friend, rather than foe. The team showed how the vaccine could successfully stop the autoimmune reaction associated with a multiple-sclerosis-like disease.
“In the past, we showed that we could use this approach to prevent autoimmunity,” said Jeffrey Hubbell, the Eugene Bell Professor in Tissue Engineering and lead author of the new paper. “But what is so exciting about this work is that we have shown that we can treat diseases like multiple sclerosis after there is already ongoing inflammation, which is more useful in a real-world context.”
First Genetic Clue Why Some People Do Not Get Sick From Covid | Barron's
Out of that group, 136 saw no Covid symptoms two weeks before and after testing positive.
One in five of that group carried at least one copy of an HLA variant called HLA-B*15:01.
Those fortunate enough to have two copies of the gene -- one from their mother, one from their father -- were over eight times more likely to be asymptomatic from Covid than other people, the study said.
Exercise post-vaccine bumps up antibodies, new study finds -- ScienceDaily
In the newly published study, participants who cycled on a stationary bike or took a brisk walk for an hour-and-a-half after getting a jab produced more antibodies in the following four weeks compared to participants who sat or continued with their daily routine post-immunization. The researchers found similar results when they ran an experiment with mice and treadmills.
Antibodies are essentially the body's "search and destroy" line of defense against viruses, bacteria, fungi and parasites. Vaccines help the immune system learn how to identify something foreign and respond by bolstering the body's defenses, including an increase in antibodies.
New study suggests two paths toward 'super immunity' to COVID-19: Research compares routes to immunity involving vaccination -- ScienceDaily
"It makes no difference whether you get infected-and-then-vaccinated, or if you get vaccinated-and-then-a-breakthrough infection," said co-senior author Fikadu Tafesse, Ph.D., assistant professor of molecular microbiology and immunology in the OHSU School of Medicine. "In either case, you will get a really, really robust immune response -- amazingly high."
Researchers find surprising benefit to the immune system following infection -- ScienceDaily
"Now we know that when you have these fairly substantial infections, interferon type 1 molecules are making the MHC and Interleukin 7 signals stronger, more abundant and more available to naïve T cells. It has never been shown that an infection can do something like this," Dr. Nikolich-Žugich said. "This study showed that an infection not only better maintained the number of naïve T cells, but it put them on a slightly higher state of alertness."
Could playing host to hookworms help prevent aging? -- ScienceDaily
They reveal how the loss of helminths has so far been linked to a range of inflammatory diseases, including asthma, atopic eczema, inflammatory bowel disease, multiple sclerosis, rheumatoid arthritis and diabetes. Some studies have shown that natural infection with helminths can alleviate disease symptoms, for example in multiple sclerosis and eczema, while other studies in animal models suggest that intentional infection with helminths could have benefits against disease.
The safer, and perhaps more palatable, option is the concept of using helminth-derived proteins to achieve the same therapeutic benefits. This was tested recently in mice and shown to prevent the age-related decline in gut barrier integrity usually seen with a high-calorie diet. It also had beneficial effects on fat tissue, which is known to be a major source of inflammageing.
Protective immunity against SARS-CoV-2 could last eight months or more: Why declining antibodies don't spell disaster for long-lasting immunity -- ScienceDaily
"It is possible that immune memory will be similarly long lasting similar following vaccination, but we will have to wait until the data come in to be able to tell for sure," says Weiskopf. "Several months ago, our studies showed that natural infection induced a strong response, and this study now shows that the responses lasts. The vaccine studies are at the initial stages, and so far have been associated with strong protection. We are hopeful that a similar pattern of responses lasting over time will also emerge for the vaccine-induced responses."
Rupert Beale · Short Cuts: How to Block Spike · LRB 21 May 2020
There are four ‘seasonal’ coronaviruses – 229E, OC43, NL63 and HKU1 – that cause mild disease in nearly everyone, only occasionally causing pneumonia. They can be given to healthy volunteers to study the immune response. They cause the ‘common cold’, and in experimentally infected humans they give rise to an antibody response. That response wanes after a few months, and the same people can be experimentally reinfected, though they tend to get milder symptoms the second time round. It is thought that adults get reinfected on average about once every five years. Sars-CoV-2 causes mild disease in most cases, and gives rise to antibody responses in nearly all cases. We don’t know how long these responses will last, but it is likely that people who suffer only mild disease will be susceptible to reinfection after a few months or years. Humanity has never developed ‘herd immunity’ to any coronavirus, and it’s unlikely that Sars-CoV-2 infection will be any different. If we did nothing, a likely possibility is that Covid-19 would become a recurring plague. We don’t know yet. It may have seemed like an aeon, but we have been aware of this virus for only a few months.
Muscles support a strong immune system -- ScienceDaily
"If the T-cells, which actively fight the infection, lose their full functionality through continuous stimulation, the precursor cells can migrate from the muscles and develop into functional T-cells," said Jingxia Wu, lead author of the study. "This enables the immune system to fight the virus continuously over a long period."
So could regular training strengthen the immune system? "In our study, mice with more muscle mass were better able to cope with chronic viral infection than those whose muscles were weaker. But whether the results can be transferred to humans, future experiments will have to show," explains Guoliang Cui.
Too much salt weakens the immune system: A diet rich in salt weakens the antibacterial immune defense -- ScienceDaily
However, other parts of the body are not exposed to the additional salt consumed with food. Instead, it is filtered out by the kidneys and excreted in the urine. And this is where the second mechanism comes into play: The kidneys have a sodium chloride sensor that activates the salt excretion function. As an undesirable side effect, however, this sensor also causes so-called glucocorticoids to accumulate in the body. And these in turn inhibit the function of granulocytes, the most common type of immune cell in the blood.
Granulocytes, like macrophages, are scavenger cells. However, they do not attack parasites, but mainly bacteria. If they do not do this to a sufficient degree, infections proceed much more severely. "We were able to show this in mice with a listeria infection," explains Dr. Jobin. "We had previously put some of them on a high-salt diet. In the spleen and liver of these animals we counted 100 to 1,000 times the number of disease-causing pathogens." Listeria are bacteria that are found for instance in contaminated food and can cause fever, vomiting and sepsis. Urinary tract infections also healed much more slowly in laboratory mice fed a high-salt diet.
Gut reaction: How immunity ramps up against incoming threats -- ScienceDaily
Eating causes a hormone called VIP to kickstart the activity of immune cells in response to potentially incoming pathogens or 'bad' bacteria. The researchers also found that immunity increased at anticipated mealtimes indicating that maintaining regular eating patterns could be more important than previously thought.
With the rise in conditions associated with chronic inflammation in the gut, such as irritable bowel and Crohn's disease, a better understanding of the early protective mechanisms governing gut health could help researchers to develop prevention strategies against unwanted inflammation and disease.
"Our study shows that T cells are more prone to be activated at certain times of the day. Identifying the mechanisms through which the biological clock modulates the T cell response will help us better understand the processes that regulate optimal T cell responses. This knowledge will contribute to improving vaccination strategies and cancer immune therapies," states Nathalie Labrecque, Professor at the Departments of Medicine and Microbiology, Infectious Diseases and Immunology at Université de Montréal.
Microbiota-Nourishing Immunity: A Guide to Understanding Our Microbial Self - ScienceDirect
Here we discuss the concept of microbiota-nourishing immunity, a host-microbe chimera composed of the microbiota and host factors that shape the microbial ecosystem, which functions in conferring colonization resistance against pathogens. We propose that dysbiosis is a biomarker of a weakening in microbiota-nourishing immunity and that homeostasis can be defined as a state of immune competence.
Study links fluorescent lighting to inflammation and immune response - Neuroscience News
“In this report, we show genome-wide changes of gene expression patterns in skin, brain and liver for two commonly utilized fish experimental models (zebrafish and Japanese rice fish, also known as medaka), and a mammalian (mice), following exposure to 4,100 K ‘cool-white’ fluorescent light,” Walter said. “In spite of the extreme divergence of these animals (i.e., estimated divergence of mice and fish about 450 million years), and drastically different lifestyles (i.e., diurnal fish and nocturnal mice), the same highly conserved primary genetic response that involves activation of inflammation and immune pathways as part of an overall acute phase response was observed in the skin, brain and liver of all three animals. Follow-up studies to further define this response in mice are underway.”
Vitamin D study sheds light on immune system effects -- ScienceDaily
In healthy people, T cells play a crucial role in helping to fight infections. In people with autoimmune diseases, however, they can start to attack the body's own tissues.
By studying cells from mice and people, the researchers found vitamin D caused dendritic cells to produce more of a molecule called CD31 on their surface and that this hindered the activation of T cells.
The team observed how CD31 prevented the two cell types from making a stable contact -- an essential part of the activation process -- and the resulting immune reaction was far reduced.
Researchers say the findings shed light on how vitamin D deficiency may regulate the immune system and influence susceptibility to autoimmune diseases.
Birch pollen allergen immunotherapy normalizes nasal gene-expression and microbial community -- ScienceDaily
In total, 44 nasal brushings were subjected to RNA-sequencing analysis to find gene expression and microbial community changes driven by allergic rhinitis and allergen immunotherapy.
According to the results, the group who started allergen immunotherapy showed decreased symptom score and reprogramming of nasal epithelial transcriptome, set of RNA molecules, during the pollen season.
"The immunotherapy affected asthma-, chemokine signaling-, and toll like receptor signaling pathways in the spring. No major differential expression was found between the two winters in any group," says researcher Sanna Toppila-Salmi from the University of Helsinki and Helsinki University Hospital.
The results also indicated that microbial community diversity of the group that underwent allergen immunotherapy approached that of the healthy controls.
Scientists Crack A 50-Year-Old Mystery About The Measles Vaccine : Goats and Soda : NPR
Well, say you get the chicken pox when you're 4 years old. Your immune system figures out how to fight it. So you don't get it again. But if you get measles when you're 5 years old, it could wipe out the memory of how to beat back the chicken pox. It's like the immune system has amnesia, Mina says.
"The immune system kind of comes back. The only problem is that it has forgotten what it once knew," he says.
So after an infection, a child's immune system has to almost start over, rebuilding its immune protection against diseases it has already seen before.
This idea of "immune amnesia" is still just a hypothesis and needs more testing, says epidemiologist William Moss, who has studied the measles vaccine for more than a decade at Johns Hopkins University.
Immune cells destroy healthy brain connections, diminish cognitive function in obese mice: Obesity may drive microglia into a synapse-eating frenzy that leads to cognitive impairment -- ScienceDaily
Nearly two billion adults worldwide are overweight, more than 600 million of whom are obese. In addition to increasing risk of conditions such as diabetes and heart disease, obesity is also a known risk factor for cognitive disorders including Alzheimer's disease. The cellular mechanisms that contribute to cognitive decline in obesity, however, are not well understood.
Elise Cope and colleagues replicated previous research by demonstrating diet-induced obesity in mice impairs performance on cognitive tasks dependent on the hippocampus and results in loss of dendritic spines -- the neuronal protrusions that receive signals from other cells -- and activates microglia. Using genetic and pharmacological approaches to block microglial activity, the researchers established microglia are causally linked to obesity-induced dendritic spine loss and cognitive decline. The results suggest obesity may drive microglia into a synapse-eating frenzy that contributes to the cognitive deficits observed in this condition.
Insulin gives an extra boost to the immune system -- ScienceDaily
"We have identified one of metabolism's most popular hormones, specifically the insulin signaling pathway, as a novel 'co-stimulatory' driver of immune system function," says Dr. Dan Winer, who is also Assistant Professor, Department of Laboratory Medicine and Pathobiology at University of Toronto. "Our work characterizes the role of this signaling pathway in immune cells, mainly T cells, opening up avenues in the future to better regulate the immune system."
Can You Cure Lyme disease? The Controversy Around Diagnosis and Treatment
In my experience, 18 months of ozone therapy was the magic bullet against Lyme disease. Ozone inactivates bacteria, viruses, fungi, yeast and protozoa by breaking through the cell wall which weakens the cell, making way for your own immune cells to move in and do their thing. It also uses extra oxygen to activate the immune system.[8] You’ll need a functional medicine doctor to put you on a program.
If you’re frustrated by Lyme disease or any chronic illness, join the club. But, don’t stay for long. The best thing you can do is arm yourself with information and seek the guidance of medical professionals who are qualified and experienced in treating the tough stuff. It takes work, but you’ll come out on the other side stronger than ever.
The immune system and the pathogenesis of depression
There is bidirectional communication between the HPA axis and the immune system. Cytokines activate the HPA axis and thus lead to the release of cortisol, the stress hormone, which ordinarily suppresses the immune response. Cortisol also inhibits its own release and thus the body is able to maintain a stable immune response through a tightly regulated feedback inhibition system. This regulation mechanism seems to be dysfunctional in depressive disorders and is thought to occur because of cytokine mediated receptor resistance to cortisol, thus impairing feedback inhibition. This essentially means that cytokines make cortisol unable to act on the receptors that would inhibit its release. Long story short — the HPA axis is hyperactive because of cytokines, leading to a chronic stress response because cytokines impair the body’s ability to regulate it — thus leading to depressive symptoms.
Probiotic Shot May Alleviate Brain Stress | GEN
Studies have also shown that patients with anxiety- and trauma-related conditions have reduced numbers of regulatory T cells (Tregs, while research also suggests that trauma, illness, or surgery can sensitize certain regions of the brain to mount an inflammatory response to subsequent stressors, which can lead to mood disorders.
“There is a robust literature that shows if you induce an inflammatory immune response in people, they quickly show signs of depression and anxiety," says lead author Matthew Frank, Ph.D., a senior research associate in the department of psychology and neuroscience. "Just think about how you feel when you get the flu."
Beyond killing tuberculosis: How can we tolerate an infection without eliminating a pathogen? -- ScienceDaily
"In contrast to conventional thinking, we show that T cells are essential for regulating the body's toler-ance to Mtb infection," explains one of the study's first authors, Dr. Nargis Khan, who is currently a postdoctoral fellow in Dr. Divangahi's lab at the RI-MUHC.
Giving the widespread drug resistance to various Mtb strains the limited pipeline of effective antibiotics and the lack of an efficient vaccine, alternative approaches to treat TB are urgent. "If we could understand the mechanisms of 'natural immunity' that controls TB in 90-95 per cent of infected individuals," says Dr. Divangahi,"we will able to design a novel therapy or vaccine to substantially reduce the world wide burden of this ancient disease."
A gut bacterium's guide to building a microbiome: Unlike invading pathogens, which are attacked by the immune system, certain good bacteria in the gut invite an immune response in order to establish robust gut colonization -- ScienceDaily
The particular species is found abundantly in the large intestines of many mammals, including humans, and was previously shown by the Mazmanian lab to protect mice from certain inflammatory and neurological disorders such as inflammatory bowel disease and multiple sclerosis. Interestingly, though there are multiple strains of B. fragilis, healthy people form a long-term, monogamous relationship with only a single strain.
"Studies by other labs have shown that most people carry the same strain of B. fragilis throughout their lives," says Donaldson. "We wanted to understand at a molecular level how these bacteria are able to colonize the gut in a stable, long-term way."
First, the researchers aimed to examine B. fragilis's symbiotic relationship with the gut by physically looking at the locations where the bacteria reside. Using electron microscopy imaging on samples of mouse intestines, the team was able to see that B. fragilis clumps together in aggregates deep within the thick layer of mucus lining the gut, nestled close to the epithelial cells that line the surface of the intestine. Donaldson and his collaborators theorized that this spatial niche is necessary for a single species to settle in and establish a stable foothold.
The team next aimed to determine what mechanisms allow B. fragilis to colonize such a niche within the gut. They found that each B. fragilis bacterium is encased in a thick capsule made of carbohydrates. The capsule is typically associated with pathogens (bad bacteria) attempting to cloak themselves from recognition by and attack from the body's immune system. Mutant bacteria lacking this capsule cannot aggregate and do not inhabit the mucosal layer. Thus, the researchers theorized that capsular carbohydrates are necessary for B. fragilis strains to monopolize their niche in the gut.
Because bacterial capsules were known to be related to an immune response in pathogenic bacteria, Donaldson and Mazmanian hypothesized that there may also be an immune response to the B. fragilis capsule. Indeed, they found that antibodies, immune proteins that grab onto and mark specific bacteria or viruses for other immune cells to engulf and destroy, were binding to the B. fragilis capsule in the intestine. One particular kind of antibody, immunoglobulin A or IgA, is found throughout the gut -- in fact, it is the most abundantly produced type of antibody in humans -- but its specific functions have been enigmatic.
