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Macrophage apoptosis in microbial infections

Published online by Cambridge University Press:  01 December 1997

H. HILBI ,
A. ZYCHLINSKY  and
P. J. SANSONETTI
H. HILBI
Affiliation:
The Skirball Institute, Department of Microbiology and Kaplan Cancer Center, New York University School of Medicine, 540 First Avenue, New York, NY 10016 USA
A. ZYCHLINSKY
Affiliation:
The Skirball Institute, Department of Microbiology and Kaplan Cancer Center, New York University School of Medicine, 540 First Avenue, New York, NY 10016 USA
P. J. SANSONETTI
Affiliation:
Unité de Pathogenie Microbienne Moleculaire, Unité 389 Institut National de la Santé et de la Recherche Médicale, Institut Pasteur, 28 rue du Dr. Roux, F-75724 Paris Cédex 15, France
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Abstract

Upon infection with a pathogen, eukaryotic cells can undergo programmed cell death as an ultimate response. Therefore, modulation of apoptosis is often a prerequisite to establish a host-pathogen relationship. Some pathogens kill macrophages by inducing apoptosis and thus overcome the microbicidal arsenal of the phagocyte. Apoptotic macrophages, on the other hand, can elicit an inflammation by secretion of proinflammatory cytokines. Shigella flexneri, the aetiological agent of bacillary dysentery, induces apoptosis in macrophages which, in agony, specifically release mature interleukin-1β (IL-1β). This cytokine attracts neutrophils (PMN) to the site of infection resulting in the massive colonic inflammation characteristic of bacillary dysentery. Shigellosis represents a paradigm of a proinflammatory apoptosis in a bacterial infection. The molecular link between apoptosis and inflammation is interleukin-1β converting enzyme (ICE) which is activated during macrophage apoptosis and binds to IpaB, a secreted Shigella protein.

Keywords

Bacteriapathogenicitymacrophagesapoptosisinflammationparasites
Type
Research Article
Information
Parasitology , Volume 115 , Issue 7 , December 1997 , pp. 79 - 87
Copyright
© 1997 Cambridge University Press

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