Interactions of enteric pathogens with human epithelial cells. Bacterial exploitation of host processes.
Many bacterial pathogens interact with surfaces on the body resulting in disease. These interactions are usually tightly regulated. Several of these pathogens also exploit host processed which contribute to their pathogenesis. Enteropathogenic existing epithelial cells using sophisticated mechanisms that exploit existing epithelial signal transduction pathways and host cytoskeleton components. Unlike EPEC, Salmonella species actually enter into epithelial cells (invade) and function as intracellular parasites. During invasion Salmonella exploit various host signal transduction pathways and cause cytoskeletal rearrangements. Salmonella enter an intracellular vacuole which remains separated from the main epithelial cell, Salmonella species trigger the formation of a novel intracellular organelle which is associated with intracellular growth. Comparison of the virulence mechanisms used by these two pathogens and their exploitation of epithelial cells illustrates several principles used by bacterial pathogens to cause disease.
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Biotechnology Laboratory, University of British Columbia, Vancouver, Canada.
D000818:Animals; D002118:Calcium / Q000502:physiology; D003599:Cytoskeleton / Q000648:ultrastructure; D004848:Epithelium / Q000382:microbiology*; D004926:Escherichia coli / Q000472:pathogenicity*; D006801:Humans; D012486:Salmonella typhimurium / Q000254:growth & development / Q000472:pathogenicity*; D015290:Second Messenger Systems; D015398:Signal Transduction
D002118:Calcium