Salmonella finds a way: Metabolic versatility of Salmonella enterica serovar Typhimurium in diverse host environments

摘要

Infection with nontyphoidal Salmonella strains, such as Salmonella enterica serovar Typhimurium (S. Typhimurium) commonly causes foodborne bacterial gastroenteritis. Studies on the pathogenesis of S. Typhimurium infection often focus on bona fide virulence factors. S. Typhimurium produces two distinct type III secretion systems that allow for the delivery of a sophisticated repertoire of effector proteins into host cells. These type III secretion systems are required for invasion of intestinal epithelial cells and subsequent replication inside professional phagocytes in the lamina propria and in deeper tissues. In immunocompetent individuals, detection of S. Typhimurium by the innate immune system results in a subacute, neutrophilic inflammatory response that confines the infection to the intestinal tract. In immunocompromised individuals, such as those with neutropenia, systemic dissemination and replication can occur. While we understand key strategies of how S. Typhimurium causes disease, we are only beginning to recognize the complex interplay of host and bacterial metabolism. Recent findings have revealed how S. Typhimurium adapts its diverse energy metabolism to mirror host metabolism and limit nutrient competition in various host niches.