The actin-polymerizing activity of SipA is not essential for Salmonella enterica serovar typhimurium-induced mucosal inflammation

Abstract

Salmonella enterica serovar Typhimurium depends on type III secretion systems to inject effector proteins into host cells to promote bacterial invasion and to induce intestinal inflammation. SipA, a type III effector, is known to play important roles in both the invasion and the elicitation of intestinal inflammation. The actin-modulating activity of SipA hasbeen shown to promote Salmonella entry into epithelial cells. To investigate whether the actin-modulating activity of SipAis required for its ability to induce an inflammatory response in vivo, we generated the SipAK635A E637W mutant, which is deficient in actin-modulating activity. Salmonella strains expressing the chromosomal SipAK635A E637W point mutation had reduced invasion abilities but still caused colitis similar to that caused by the wild-type strain in a mouse model of infection. Our data indicate that the SipA actinpolymerizing activity is not essential for the SipA-induced inflammatory response in the mouse model of infection. © 2013, American Society for Microbiology.