Salmonella Typhimurium and inflammation: a pathogen-centric affair

Microbial infections are controlled by host inflammatory responses that are initiated by innate immune receptors after recognition of conserved microbial products. As inflammation can also lead to disease, tissues that are exposed to microbial products such as the intestinal epithelium are subject to stringent regulatory mechanisms to prevent indiscriminate signalling through innate immune receptors. The enteric pathogen Salmonella enterica subsp. enterica serovar Typhimurium, which requires intestinal inflammation to sustain its replication in the intestinal tract, uses effector proteins of its type III secretion systems to trigger an inflammatory response without the engagement of innate immune receptors. Furthermore, S. Typhimurium uses a different set of effectors to restrict the inflammatory response to preserve host homeostasis. The S. Typhimurium-host interface is a remarkable example of the unique balance that emerges from the co-evolution of a pathogen and its host. In this Review, Galan discusses the mechanisms by which Salmonella enterica subsp. enterica serovar Typhimurium triggers inflammation in the intestinal tract through the activities of effector proteins as well as the mechanisms that are aimed at recovering host homeostasis after the inflammatory response.

Automated summary

Microbial infections are controlled by host inflammatory responses initiated by innate immune receptors recognizing microbial products. The enteric pathogen Salmonella Typhimurium triggers inflammation in the intestinal tract using effector proteins without engaging innate immune receptors, while also employing other effectors to restrict the inflammatory response and preserve host homeostasis. The interaction between S. Typhimurium and its host represents a unique balance achieved through co-evolution, with mechanisms aimed at recovering host homeostasis after the inflammatory response.