Shigella-induced apoptosis is dependent on caspase-1 which binds to IpaB

J Biol Chem. 1998 Dec 4;273(49):32895-900. doi: 10.1074/jbc.273.49.32895.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis*
  • Bacterial Proteins / metabolism*
  • Caspase 1 / genetics
  • Caspase 1 / metabolism*
  • Macrophages, Peritoneal / enzymology
  • Macrophages, Peritoneal / microbiology
  • Mice
  • Mice, Knockout
  • Protein Binding
  • Proto-Oncogene Proteins c-bcl-2 / physiology
  • Shigella / physiology*
  • Tumor Suppressor Protein p53 / physiology

Substances

  • Bacterial Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53
  • ipaB protein, Shigella
  • Caspase 1