Characterisation of SteA, and effetor of Salmonella typhimurium

Abstract

Salmonella typhimurium causes self-limiting gastroenteritis in humans and typhoid like condition in mice. S. typhimurium actively invades and infects intestinal epithelial cells. Various stages of infection are regulated by type three secretion systems encoded on different Salmonella pathogenicity islands (SPIs) which translocate effector proteins. They are secreted via the specific secretion systems directly into the host cytoplasm. These effectors are essential for virulence of the bacteria and regulate various host cell responses to help in a successful infection and further dissemination to other tissues. Salmonella translocated effector A (SteA) is an effector protein of S. typhimurium regulated by both SPI-I and SPI-II. In this report we have found that ∆SteA results in a heightened immune response by affecting IκB.