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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Vitamin D supplements could ease irritable bowel syndrome

Vitamin D supplements could ease painful Irritable Bowel Syndrome IBS symptoms. Scientists from the University's Department of Oncology and Metabolism reviewed and integrated all available research on vitamin D and IBS. The study showed a high prevalence of vitamin D deficiency in IBS patients. They also assessed the possible benefits of vitamin D supplements on IBS symptoms. Their findings suggested supplements may help to ease symptoms which can include abdominal pain, bloating, diarrhea and constipation. Vitamin D was shown to have the most benefit on quality of life in IBS.

People with IBS should have their vitamin D levels tested and a large majority of them would benefit from supplements. IBS is a poor condition which impacts severely on the quality of life of sufferers. There is no single known cause and no cure. IBS is a debilitating functional disorder of the gastrointestinal (GI) tract. Little is known about why and how the condition develops, although it is known that diet and stress can make symptoms worse.

Vitamin D is essential for general wellbeing, including bone health, immune function, mental health as well as gut health. Vitamin D inadequacy can be remedied relatively easily with supplements if diagnosed. Low vitamin D status has already been associated with the risk of colorectal cancer and has been implicated in inflammatory bowel disease.
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High salt diet hobbles the brain

A new study has shown that mice fed with a very high-salt diet experienced declined blood flow to their brain, the integrity of blood vessels in the brain suffered, and performance on tests of cognitive function plummeted.

Researchers found that those effects were not as long has been widely believed, a natural consequence of high blood pressure. Instead, they appeared to be the result of signals sent from the gut to the brain by the immune system.

The study, conducted by researchers at Weill Cornell Medicine in New York. The research sheds light on a subject of keen interest to scientists exploring the links between what we eat and how well we think, and the mediating role that the immune system plays in that communication.

This suggests that even before a chronic high-salt diet nudges blood pressure up and compromises the health of tiny blood vessels in the brain, the oversalted gut is independently sending messages that lay the groundwork for corrosion throughout the vital network.

In the small intestines of mice, the authors of the new research found that a very high-salt diet prompted an immune response that boosted circulating levels of an inflammatory substance called interleukin-17. These high levels of IL-17 set off a cascade of chemical responses inside the delicate inner linings of the brain's blood vessels.

The result in mice fed with the high-salt diet: blood supply to two regions crucial for learning and memory-the cortex and hippocampus slowed markedly. And mental performance slid. Compared to mice fed a diet lower in salt, the maze-running skills of the mice who consumed high-salt levels faltered, and they failed to respond normally to whisker stimulation, or a new object in their cage.

In mice, that evidence of cognitive impairment was apparent even in the absence of high blood pressure. The immune system's role in sending signals between brain and gut is also seen in diseases like multiple sclerosis, rheumatoid arthritis, psoriasis and inflammatory bowel disease-all disorders that are linked to poor functioning of the brain's blood vessels.
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Smoking may cause inflammatory bowel disease

Exposing mice to cigarette smoke results in colitis, an inflammation of the colon resembling Crohn's disease, and identify a specific white blood cell and inflammatory protein responsible for this effect. Previous research shows that smoking significantly increases the risk of Crohn's disease, an inflammatory bowel disease. However the mechanism by which cigarette smoke affects the gastrointestinal system was not known.

One possibility is that inflammation in the lungs caused by smoking could have a knock-on effect in the intestine.
a connection between the lung and the large intestine has long been emphasized. Crohn's disease may occur in people with airway diseases, suggesting that inflammation in the lungs is linked with inflammation in the gut.

Researchers exposed mice to smoke from twenty cigarettes a day, six days a week, for a few weeks. The researchers then examined the presence of inflammation in the mice's lungs and colons. Mice exposed to cigarette smoke showed significant inflammation in their lungs. Interestingly, they also suffered from a type of colitis resembling Crohn's disease.

The researchers found increased levels of mucus and inflammation in the colon, and blood in the feces of the smoke-exposed mice. They also found increased levels of CD4+ T cells, a type of white blood cell, which were releasing a pro- inflammatory protein called interferon-gamma. Cigarette smoking activates specific white blood cells in the lung, which might move to the colon, triggering bowel inflammation.
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