Salmonellosis continues to be a major worldwide health concern. Essential to the pathogenicity of these bacteria is a type III protein secretion system (TTSS) encoded within a pathogenicity island (SPI-1) located at centisome 63. This system directs the translocation into host cells of a battery of bacterial effector proteins that stimulate a variety of cellular responses. These responses are critical for pathogenicity as they allow the bacteria to gain access to host cells, avoid host defense mechanisms and reach deeper tissues. Work in our laboratory supported by this Grant has focused on the study of the cell biology of the complex functional interface between Salmonella enterica and host cells. The proposed research project is aimed at gaining a better understanding of the cell biology of the Salmonella host interactions and the function of several SPI-1 TTSS effector proteins whose role in the infection process is poorly understood. More specifically, we propose: 1) To elucidate cellular events that lead to Salmonella-induced actin polymerization and bacterial entry; 2) To investigate the role of the SP1-TTSS effector protein SopB in the formation of the Salmonella-containing macropinosomes; 3) To investigate the effector function of the SPI-1 TTSS secreted protein SipB; and 4) To investigate the potential role of the SPI-1 TTSS in the interaction of Salmonella with the innate immune system. These studies will advance the understanding of the cell biology of Salmonella enterica infections and that of other important pathogens that have evolved close associations with their hosts. ? ?
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