Rapidly induced fucosylation of intestinal epithelium sustains host-commensal symbiosis during sickness.

ABSTRACT: Systemic infection induces conserved physiological responses that include both resistance and ‘tolerance of infection’ mechanisms. Among these responses, temporary anorexia associated with an infection is often beneficial. It poses, however, a problem for the trillions of microbes residing in the gastrointestinal tract, as they also experience reduced substrate availability. We hypothesized that under anorectic conditions caused by infection, the host might activate protective mechanisms to support the gut microbiota during the acute phase of the disease. Here, we report that systemic exposure to Toll-like receptor (TLR) ligands causes rapid α1,2-fucosylation of the small intestine epithelial cells (IEC). The process requires sensing of TLR agonists and production of IL-23 by dendritic cel

ORGANISM(S): mouse gut metagenome

SUBMITTER: Peter Turnbaugh 

PROVIDER: E-GEOD-60874 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress