Salmonella typhimuriumdisseminates within its host by manipulating the motility of infected cells

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Abstract
The mammalian host has a number of innate immune mechanisms designed to limit the spread of infection, yet many bacteria, includingSalmonella, can cause systemic disease.Salmonella typhimurium-infected phagocytes traverse the gastrointestinal (GI) epithelium and enter the bloodstream within minutes after ingestion, thereby spreading throughout its host. Here, we provide a cellular and molecular basis for this phenomenon. We demonstrate thatS. typhimuriummanipulates the migratory properties of infected GI phagocytes with a type III secretion system. We show that one secreted effector, SrfH, interacts with the host protein TRIP6, a member of the zyxin family of adaptor proteins that regulate motility. SrfH promotes phagocyte motilityin vitroand accelerates the systemic spread of infection away from the lumen of the intestine in the mouse. This is a previously uncharacterized mechanism by which an intracellular pathogen overcomes host defenses designed to immobilize infected cells.