| Literature DB >> 9830039 |
H Hilbi1, J E Moss, D Hersh, Y Chen, J Arondel, S Banerjee, R A Flavell, J Yuan, P J Sansonetti, A Zychlinsky.
Abstract
We report here that the Shigella invasion plasmid antigen (Ipa)B, which is sufficient to induce apoptosis in macrophages, binds to caspase (Casp)-1, but not to Casp-2 or Casp-3. Casp-1 is activated and its specific substrate interleukin-1beta is cleaved shortly after Shigella infection. Macrophages isolated from Casp-1 knock-out mice are not susceptible to Shigella-induced apoptosis, although they respond normally to other apoptotic stimuli. Shigella kills macrophages from casp-3, casp-11, and p53 knock-out mice as well as macrophages overexpressing Bcl-2. We propose that Shigella induces apoptosis by directly activating Casp-1 through IpaB, bypassing signal transduction events and caspases upstream of Casp-1. Taken together these data indicate that Shigella-induced apoptosis is distinct from other forms of apoptosis and seems uniquely dependent on Casp-1.Entities:
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Year: 1998 PMID: 9830039 DOI: 10.1074/jbc.273.49.32895
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157