Mechanisms and consequences of intestinal dysbiosis.

The composition of the gut microbiota is in constant flow under the influence of factors such as the diet, ingested drugs, the intestinal mucosa, the immune system, and the microbiota itself. Natural variations in the gut microbiota can deteriorate to a state of dysbiosis when stress conditions rapidly decrease microbial diversity and promote the expansion of specific bacterial taxa. The mechanisms underlying intestinal dysbiosis often remain unclear given that combinations of natural variations and stress factors mediate cascades of destabilizing events. Oxidative stress, bacteriophages induction and the secretion of bacterial toxins can trigger rapid shifts among intestinal microbial groups thereby yielding dysbiosis. A multitude of diseases including inflammatory bowel diseases but also metabolic disorders such as obesity and diabetes type II are associated with intestinal dysbiosis. The characterization of the changes leading to intestinal dysbiosis and the identification of the microbial taxa contributing to pathological effects are essential prerequisites to better understand the impact of the microbiota on health and disease.

The role of milk sialyllactose in intestinal bacterial colonization.

Milk oligosaccharides influence the composition of intestinal microbiota and thereby mucosal inflammation. Some of the major milk oligosaccharides are α2,3-sialyllactose (3SL) and α2,6-sialyllactose, which are mainly produced by the sialyltransferases ST3GAL4 and ST6GAL1, respectively. Recently, we showed that mice fed milk deficient in 3SL were more resistant to dextran sulfate sodium-induced colitis. By contrast, the exposure to milk containing or deficient in 3SL had no impact on the development of mucosal leukocyte populations. Milk 3SL mainly affected the colonization of the intestine by clostridial cluster IV bacteria.