Immune signature predicts asthma susceptibility

Asthma is a chronic inflammatory disease driven by the interplay of genetics, environmental factors and a diverse cast of immune cells. Researchers at La Jolla Institute for Allergy and Immunology (LJI) identified a subset of T cells, whose frequency serves as early childhood immune signature that predicts the risk of developing asthma later on.

Children who, at the age of one, had a higher frequency of MAIT cells appear to be less likely to develop asthma by the age of seven. Consistent with the "hygiene hypothesis," which holds that increased microbial exposure in the first years of life is protective for asthma, the team's findings also indicate that the presence of house dust components that stimulate the innate immune system decreases asthma risk.

Unlike conventional T cells, which belong to the adaptive arm of the immune response and take a few days before they are fully trained on a single, specific protein fragment or peptide antigen, MAIT and iNKT cells recognize molecular components common to many microbes. The team analyzed the frequency of different types of immune cells in blood collected from 110 one year-old study participants, the presence of immune-stimulatory components in the subjects' house dust and asked whether any of the factors correlated with an increased of asthma at age seven.

Certain immune signatures such as having more MAITs that are protective in humans MAIT cells are unique in that they are borne to make gamma interferon, which could help skew the immune system toward an asthma-protective. And while the absolute numbers of iNKT cells had no bearing on asthma risk, the iNKT cell antigenic content in house dust from subjects' houses did. iNKT activity reflects a home environment with increased microbe exposure and prevents asthma.
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Gut bacteria could be good or bad

Bacteria that live in and on human body are emerging as an increasingly important player in health and wellness. Human co-existence with these organisms is complex, minor changes in this relationship can leads to adverse reaction on human health.

Researchers from the University of Rochester Medical Center found that impairing a rare group of cells in the small intestine allows gut bacteria to invade the organ and cause major inflammation. The study was conducted in mice, but has implications for the treatment of inflammatory bowel disease (IBD), a group of disorders characterized by chronic inflammation in the digestive track.

Keeping guts in good shape requires the cooperation of multiple intestinal cells with the bacteria that live around them. Though small in number, intestinal cells called Paneth cells play an important role; they make antimicrobial compounds that keep bacteria in check and help form the lining of the small intestine, a physical barrier between the organ and the resident bacteria.

Previous research shows that changes or mutations in Paneth cells are associated with increased inflammation, including in individuals with Crohn's disease, a type of IBD. But, scientists were unsure how Paneth cells opened the door to inflammatory damage.

Researchers led by Felix O. Yarovinsky, M.D. found the answer in a process called autophagy, which helps cells remove unwanted cellular material or debris. His team turned off autophagy in Paneth cells in mice and then exposed them to a stressor-a parasite called Toxoplasma gondii. Without autophagy, the barrier between the small intestine and the gut bacteria broke down; bacteria invaded the organ and caused severe infection and inflammation.

Paneth cells are like the guardians of the intestine and autophagy is like their armor, when their  armor were removed, the Paneth cells couldn't control the intestinal bacteria and it went wild, causing severe disease. The study suggests that normal autophagy in Paneth cells is required to regulate bacteria in the gut, keeping it at bay and preventing the gut bacteria from invading host tissue.

Paneth cells make up just 2 percent of the cells in the intestine, and the fact that restricting autophagy in these cells led to big problems was an unexpected result. Gut bacteria play a role in the development of IBD, which includes Crohn's disease and ulcerative colitis. But how bacteria in the gut are controlled in these conditions remains elusive. This study and others point to Paneth cells as key regulators of the interactions between host and gut bacteria, and further research could inform the design of future therapies.
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Links between Crohn's and Parkinson's disease

Mount Sinai Researchers have just discovered that patients in the Ashkenazi Jewish population with Crohn's disease (a chronic inflammatory of the digestive system) are more likely to carry the LRRK2 gene mutation. This gene is the major genetic cause of Parkinson's disease, which is a movement disorder.

Crohn's disease is a complex disorder with multiple genes and environmental factors involved, which disproportionally affects individuals of Ashkenazi Jewish ancestry. The presence of shared LRRK2 mutations in patients with Crohn's disease and Parkinson's disease provides refined insight into disease mechanisms and may have major implications for the treatment of these two seemingly unrelated diseases.

Researchers used international data from the last decade up to the present to analyze the occurrence of some coding genetic mutations in the human genome of many  patients with Crohn's disease and compared them to people without the disorder. They identified mutations in the LRRK2 gene that are more frequently found in Crohn's disease cases as compared to unaffected individuals.

When they discovered a link between Crohn's and the LRRK2 gene mutations they went further to assess the possible genetic link between Crohn's and Parkinson's. The team then looked at a much larger sample of people including patients with Crohn's, Parkinson's, and no disease.

The study found two mutations of the LRRK2 gene in Crohn's disease patients. One of them called the risk mutation was more common in patients with Crohn's, while the other (the protective mutation) was more prevalent in patients without the disease. Most Crohn's disease patients who carried the risk mutation developed the disease on average six years earlier than those who did not carry this mutation.

The research also shows that more Crohn's patients with the risk mutation developed the disease in the small intestine, compared to those without the mutation. If the disease starts in the small intestine, it becomes more difficult to manage and often leads to complications and surgeries.
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How to fight inflammation with exercise

Inflammation is the body's way of healing itself after an injury and protecting itself from infection; but chronic inflammation is associated with different kinds of diseases.

During exercise like running, jumping, jogging, swimming and walking muscle cells release a small protein known as Interleukin 6, IL-6, which fights an inflammation. Any forms of exercise that you can think of will produce the same Interleukin 6. It has several anti-inflammatory effects; it lowers levels of a protein called TNF alpha, which triggers inflammation in the body.

It prevents the effects of a protein known as interleukin 1 beta, which triggers inflammation that can damage the cells in the pancreas. The quantity of IL-6 release by muscles is determined by quality of time spent during exercise, the longer you engage in exercise, the more IL-6 will be released into your body.

Regular exercise induces a strong anti-inflammatory effect on the body and it prevents an inflammation. It also increases levels of protein, known as Interleukin-15 (IL-15), in muscle cells. IL-15 regulates the accumulation of abdominal fat, with higher levels of IL-15 providing protection against abdominal fat buildup.

Regular exercise should be used as part of the treatment for chronic inflammatory diseases. Exercise serves as natural, anti-inflammatory and metabolism-improving 'drug'. It can be useful for treating type 2 diabetes and cardiovascular disease.
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