Salmonella typhimurium paves its own road into target cells Dan Gordon  Gastroenterology  Volume 115, Issue 2, (August 1998) DOI: 10.1016/S0016-5085(98)70185-4 Copyright © 1998 Terms and Conditions

After S. typhimurium binds to the surface of an intestinal mucosal cell, it injects bacterial proteins through the host cell membrane by a type III secretory mechanism. One of these proteins, Sop E, causes a series of events leading to entry of the organism into the epithelial cell and ultimately to inflammation and diarrhea. Sop E seletively activates two members of the rho family of small GTP binding proteins, CDC-42 and Rac-1, that cause rearrangements of the actin cytoskeleton in the adjacent plasma membrane, leading to localized membrane ruffling and enabling the bacterium to enter the cell. Activation of CDC-42 and Rac-1 also leads to JNK-1 activation which, along with other products of the internalized S. typhimurium, induces production of cytotoxic cytokines leading to inflammation and diarrhea Gastroenterology 1998 115, DOI: (10.1016/S0016-5085(98)70185-4) Copyright © 1998 Terms and Conditions