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Shigella flexneri induces apoptosis in infected macrophages

Shigella flexneri induces apoptosis in infected macrophages THE Gram-negative bacterial pathogen Shigella flexneri causes dysentery by invading the human colonic mucosa1. Bacteria are phagocytosed by enterocytes2, escape from the phagosome into the cytoplasm3 and spread to adjacent cells4. After crossing the epithelium, Shigella reaches the lamina propria of intestinal villi, the first line of defence. This tissue is densely populated with phagocytes that are killed in great numbers, resulting in abscesses5,6. The genes required for cell invasion7 and macrophage killing2 are located on a 220-kilobase plasmid. We report here on the mechanism of cytotoxicity used by S. flexneri to kill macrophages. Each of four different strains was tested for its capacity to induce cell death. An invasive strain induced programmed cell death (apoptosis8,9), whereas its non-invasive, plasmid-cured isogenic strain was not toxic; neither was a mutant in ipa B (ref. 10) (invasion protein antigen), a gene necessary for entry. A non-invasive strain expressing the haemolysin operon of Escherichia coli 11 induced accidental cell death (necrosis), demonstrating that other bacterial cytotoxic mechanisms do not lead to apoptosis. This is the first evidence that an invasive bacterial pathogen can induce suicide in its host cells. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Springer Journals

Shigella flexneri induces apoptosis in infected macrophages

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References (18)

Publisher
Springer Journals
Copyright
Copyright © 1992 by Nature Publishing Group
Subject
Science, Humanities and Social Sciences, multidisciplinary; Science, Humanities and Social Sciences, multidisciplinary; Science, multidisciplinary
ISSN
0028-0836
eISSN
1476-4687
DOI
10.1038/358167a0
Publisher site
See Article on Publisher Site

Abstract

THE Gram-negative bacterial pathogen Shigella flexneri causes dysentery by invading the human colonic mucosa1. Bacteria are phagocytosed by enterocytes2, escape from the phagosome into the cytoplasm3 and spread to adjacent cells4. After crossing the epithelium, Shigella reaches the lamina propria of intestinal villi, the first line of defence. This tissue is densely populated with phagocytes that are killed in great numbers, resulting in abscesses5,6. The genes required for cell invasion7 and macrophage killing2 are located on a 220-kilobase plasmid. We report here on the mechanism of cytotoxicity used by S. flexneri to kill macrophages. Each of four different strains was tested for its capacity to induce cell death. An invasive strain induced programmed cell death (apoptosis8,9), whereas its non-invasive, plasmid-cured isogenic strain was not toxic; neither was a mutant in ipa B (ref. 10) (invasion protein antigen), a gene necessary for entry. A non-invasive strain expressing the haemolysin operon of Escherichia coli 11 induced accidental cell death (necrosis), demonstrating that other bacterial cytotoxic mechanisms do not lead to apoptosis. This is the first evidence that an invasive bacterial pathogen can induce suicide in its host cells.

Journal

Nature – Springer Journals

Published: Jul 9, 1992

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