by New research from Umeå University in Sweden sheds light on a previously unknown bacterium that plays a crucial role in maintaining the protective intestinal mucus barrier, even under low-fiber diets. This discovery could pave the way for innovative treatment strategies for conditions linked to Western diets, such as inflammatory bowel disease, ulcerative colitis.
Sandra Holmberg, a Ph.D. student at the Department of Molecular Biology, explains, “Our findings contribute significantly to our understanding of the intricate relationship between the intestinal bacteria and the mucus layer. This knowledge may eventually lead to new therapeutic approaches for diseases associated with the Western diet.”
The human body employs various defense mechanisms to safeguard itself against the vast array of microorganisms residing in our intestines. One of the primary protective barriers is the mucus layer that coats the intestinal wall. Typically, this mucus acts as an impenetrable shield, preventing bacteria from coming into direct contact with the intestinal wall and maintaining a healthy distance. In the large intestine, where bacterial populations are most abundant, this barrier is sustained through continuous mucus secretion by the body.
The composition of the intestinal bacterial community and the mucus barrier are influenced by diet. Previous studies have demonstrated that mice fed a Western diet, characterized by high fat, sugar, and low dietary fiber, experience alterations in their intestinal bacterial populations. Consequently, less mucus is secreted, and the remaining mucus becomes more permeable to bacteria. This heightened risk of bacterial proximity to the body can lead to infection and inflammation.
Despite the prevalence of infection and inflammation being relatively rare, the identity of the intestinal bacteria responsible for mucus regulation and the underlying mechanisms have remained elusive.
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1. Source: Coherent Market Insights, Public sources, Desk research.
2. We have leveraged AI tools to mine information and compile it.
