动物实验,肠道细菌 z-bo 2020-08-20 561

　　In order to protect the intestinal bacteria during illness, special sugars are produced in the intestines of diseased mice, which are used as food for plant flora and maintain a healthy microbial balance. This protective mechanism also seems to help with resistance to other harmful pathogens, and the destruction of these pathogens may play a role in certain human diseases such as Crohn's disease.

　　Dr. Alexander Cerbonsky, Chairman of the Immunology Committee of the University of Chicago, is the lead author of this article. He said: “In the case of illness, the host and its intestinal flora are affected, but the host protects

　　However, it damages the beneficial bacteria in the intestines and plays an important role in health and disease. In order to study the mechanisms that support the microbiome during the disease process, Chervonsky and his research team focused on the potential internal resources produced by the host L-fucose (L-fucose). Studies have confirmed that this sugar affects intestinal bacteria. The host cannot use L-fucose as an energy source, but when combined with protein, the flora can use it as a food source. Under normal circumstances, the small intestine of mice hardly produces L-fucose.

　　The research team exposed several different mice to a molecule that mimics a systemic infection. The mice are sick, eat less, drink less water, and lose weight. A few hours after the disease was induced, the researchers observed that L-fucose was produced on almost all the surface of the small intestine. This effect can only be seen in response to disease. Next, the researchers tested genetically engineered mice lacking Fut2, which are involved in the production of L-fucose. Mice lacking Fut2 remain healthy under normal conditions, but after the disease is induced, their weight recovery rate is much slower than that of normal mice. Only mice with intact intestinal flora and capable of producing L-fucose can recover effectively.

　　Chervonsky: "The mice that produce L-fucose recover faster than the mice that cannot produce L-fucose. Removing the bacteria eliminates this effect."

　　The analysis used confirmed that the production of L-fucose metabolism affects Enterobacter. They pointed out that diseased mice lacking Fut2 had significantly higher gene expression of harmful microorganisms than normal mice. The researchers speculated that the production of L-fucose somehow prevented the expression of pathogenic genes in opportunistic bacteria, exposing mice to mild bacterial pathogens and inducing the disease four days later. In this case, mice lacking Fut2 lost more weight than normal mice. This indicates that the production of L-fucose helps the host resist other harmful pathogens. Interestingly, about 20% of humans lack the functional gene that produces L-fucose. The problem is related to inflammatory bowel disease called Crohn's disease.

　　Chervonsky said: "I suspect that without L-fucose, we would not be able to prevent the activity of the genes that cause the disease. This is why bacteria play an important role in Crohn's disease. Can it be used in future treatments? Use? Need further research?"