Inflammasome activation links enteric <i>Salmonella</i> Typhimurium infection to a rapid, cytokine-dependent increase in intestinal mucin release.

ABSTRACT: The host restricts Salmonella enterica serovar Typhimurium infection of the gut via inflammasome-dependent sloughing of infected epithelial cells. Here we determined that concurrent caspase 1/11-dependent release of the goblet cell-derived mucin, Muc2, into the intestinal lumen also controls Salmonella burdens in infected mice. The increased release of mucins from goblet cells in the cecum and nearby proximal colon, and the subsequent thickening of the protective mucus barrier layer in the distal colon, were all dependent on the cytokines interleukin (IL)-18 and IL-22, as deficiencies in either cytokine resulted in reduced mucin secretion. Supplementation of IL-18 into IL-22 deficient mice restored mucin secretion, indicating that IL-22 acted upstream of IL-18 secretion durin

SUBMITTER: Han X 

PROVIDER: S-EPMC11497969 | biostudies-literature | 2024 Jan-Dec

REPOSITORIES: biostudies-literature