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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How intestine repairs itself

Researchers at Baylor College of Medicine, Johns Hopkins University School of Medicine and the University of California, San Francisco have gained new insights into how the small intestine, one of the fastest renewing tissues in the human body, repairs itself after injury caused by intestinal rotavirus infection. Their findings have led them to propose that, contrary to the current thinking, how the intestine repairs itself seems to depend on the type of damage, and they found that triggers that were previously thought to be unimportant are actually essential for repairing virus-caused injury.

They studied different damage model, damage caused by rotavirus, a common small intestinal viral infection that affects young children. Repair and turnover of the epithelium, the most external cellular layer of the small intestine responsible for absorption of nutrients and other functions, depend on the intestinal stem cells, regardless of the cause of the damage. There are two types of intestinal stem cells: CBCs (crypt-based columnar cells) and reserve intestinal stem cells. The type of injuries studied until now damages the highly proliferative CBCs, and when these stem cells are destroyed, the reserve intestinal stem cells respond to restore the damage. The response to injury caused by rotavirus, however, is different.

Rotavirus is an infection and has a very specific damage pattern, the virus specifically infects epithelial cells, but not the stem cells. The first finding refers to the type of stem cell involved in the repair of the epithelial cells damaged by the virus. Previous studies had shown that when CBC stem cells are damaged, the reserve stem cells come to their rescue leading the reconstitution of the damaged epithelium. When rotavirus damages the epithelium, but not the stem cells,  the CBCs, not the reserve stem cells, are the primary cell type involved in the restoration of the intestinal epithelium.

 CBCs were not considered important for the repair of intestinal epithelium, but the results show that they are crucial for injury repair after rotavirus-induced epithelial cell damage in contrast to previous studies supporting the reserve intestinal stem cells as the cell type involved in epithelial restitution. The second finding refers to the source of the signaling molecules-called WNTs that trigger the growth and activation of stem cells leading to injury repair. Scientists have described two sources of WNT molecules, epithelial cells and mesenchymal cells. Epithelial WNT molecules were essential to signal the stem cells to repair the damage caused by rotavirus infection.
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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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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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