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17 Induction of Apoptosis by Microbial Pathogens, Page 1 of 2
< Previous page Next page > /docserver/preview/fulltext/10.1128/9781555817633/9781555813024_Chap17-1.gif /docserver/preview/fulltext/10.1128/9781555817633/9781555813024_Chap17-2.gifAbstract:
There are two criteria to distinguish apoptosis from necrosis: morphology and DNA fragmentation. Typical morphological changes that occur during apoptosis include cell shrinkage and loss of normal cell-to-cell contacts, blebbing at the cell surface, and intense cytoplasmic vacuolization. Interestingly, the morphological changes, the fragmentation of DNA, and the expression of markers for recognition by phagocytes are very similar across different cell types and species. Caspases are a family of cysteine proteases that play a central role in the apoptotic pathway. Among cysteine proteases, caspases are unique in requiring an aspartate at the cleavage site. Bcl-2 is homologous to the Caenorhabditis elegans apoptosis inhibitor gene ced-9. bcl-2 complements the ced-9 mutation in worms and inhibits apoptosis in many different instances when overexpressed in mammalian cells. Many bacterial pathogens induce apoptosis in host cells. This chapter groups microbial pathogens by the mechanisms they use to induce apoptosis. Bordetella pertussis kills macrophages by apoptosis in vitro by secreting adenylate cyclase-hemolysin (AcHly) toxin. This toxin has two domains: (i) a potent adenylate cyclase activity, which is activated by calmodulin, and (ii) a hemolysin activity, which is a pore-forming protein that is thought to allow the translocation of the cyclase into the host cell cytoplasm.