ETEC regulates GPR109A expression in intestinal epithelial cells mediated by inflammatory factors secreted by macrophages

Abstract

Gut microbes control host immunity and homeostasis, and their abnormal changes are associated with the occurrence and development of diseases. GPR109A is an essential receptor on intestinal epithelial cells and interacts with gut microbes. Moreover, increased Enterotoxigenic Escherichia coli K88 strain colonization promotes GPR109A expression in vivo. This study evaluated the detailed mechanism of pathogenic bacteria promoting GPR109A expression. The results revealed that ETEC K88 indirectly fosters GPR109A expression in intestinal epithelial cells by stimulating the production of IL-1β and TNF-α through macrophages which are mediated by ERK1/2 pathway. The study explains the molecular mechanisms by which the bacteria regulate the homeostasis of the host intestinal gene expression during ETEC infection.

Keywords: ERK1/2 pathway; Escherichia coli K88; GPR109A; Immunity; Intestinal epithelial cells.