Importance of a Lipopolysaccharide-Initiated, Cytokine-Mediated Host DefenseMechanism in Mice against Extraintestinally Invasive Escherichia coli

摘要

Extraintestinally invasive Eschenchta coli (EC) that possess strains retrievedfrom patients with bacterem both a complete LPS and Ki capsule evade both completement -mediated bacteriolysis and neutrophil-mediated killing. Since C3H/HeJ mice that are hyporesponsive to LPS were uniquely susceptible to lethal infection with EC of this phenotype, we speculated there was an LPS-initiated host defence mechanism against this pathogenic phenotype. The LPS-normoresponsive C3H/HeN as well as the C3H/HeJ mice cleared these EC from the circulation with 4 h of intravenous administration. Whereas electron micrographs of the liver demonstrated these EC undergoing degeneration within the phagolysosomes of both macrophages and Kupffer cells of C3H/HeN mice, these EC replicated within these cells of C3H/HeJ mice occurred with activation of Kupffer cells and peritoneal macrophages in vivo with BCG and in vitro with IFY-y, but not with LPS.