Role of novel adhesins in interaction of Salmonella with the epithelium
Salmonella enterica is an important gastrointestinal pathogen of humans and animals with the ability to invade non-phagocytic cells and to persist and proliferate within mammalian cells. We recently performed the functional characterization of various new pathogenicity islands in Salmonella enterica. While analyzing the virulence functions of such invasion of non-polarized cells and intracellular replication, no specific contributions of SPI4 to SPI9 were observed. Invasion by Salmonella is commonly analyzed using non-polarized epithelial cells. Since these cells do not represent the properties of cells encountered by Salmonella in the intestinal epithelium, we hypothesized that cell culture models with polarized cells should give a natural setting for invasion experiments. Using infection models with polarized epithelial cells such as MDCK, T84 or CaCo-2, we observed that the function of SPI1 and, in addition, of SPI4 is required for efficient invasion. We found that Salmonella is unable to invade polarized epithelial cells without the function of proteins encoded by Salmonella Pathogenicity Island 4 (SPI4) (Gerlach et al., 2008) in cooperation with the SPI1-T3SS.