Molecular mechanisms of bacteria induced apoptosis.
Interaction of mammalian cells with pathogenic bacteria results in a whole variety of responses in the infected cells including internalization or phagocytosis of the bacterium, release of cytokines, secretion of defensins or production of oxygen radicals. However, recent studies pointed out that many bacteria are able to trigger apoptosis in the host cell. The induction of apoptosis upon infection results from a complex interaction of bacterial proteins with cellular proteins finally mediating apoptosis. Thus, bacteria are able to activate several pro-apoptotic proteins, e.g. caspases, to inactivate anti-apoptotic proteins, e.g. NF(kappa)B or MAP-kinases, or to upregulate endogenous receptor/ligand systems, that induce apoptosis, on the surface of the infected cell. Host cell apoptosis very often serves the bacteria to attack the host and to gain access to the tissue. However, in some infections, apoptosis of mammalian cells significantly contributes to the host defense against the bacteria further indicating the role of apoptosis in host-pathogen interactions.
Grassmé
H
H
Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Jendrossek
V
V
Gulbins
E
E
D000818:Animals; D017209:Apoptosis; D001419:Bacteria / Q000378:metabolism*; D006801:Humans; D008024:Ligands; D008928:Mitochondria / Q000378:metabolism; D008954:Models, Biological; D011485:Protein Binding; D011550:Pseudomonas aeruginosa / Q000378:metabolism; D012486:Salmonella typhimurium / Q000378:metabolism; D012763:Shigella flexneri / Q000378:metabolism; D013211:Staphylococcus aureus / Q000378:metabolism; D015008:Yersinia enterocolitica / Q000378:metabolism; D015010:Yersinia pestis / Q000378:metabolism; D015011:Yersinia pseudotuberculosis / Q000378:metabolism
D008024:Ligands