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Interleukin 1 is released by murine macrophages during apoptosis induced by Shigella flexneri

A Zychlinsky1, C Fitting, J M Cavaillon

  • 1Unité de Pathogénie Microbienne Moléculaire, Institut National de la Santé et de la Recherche Médicale U389, Institut Pasteur, Paris, France.

The Journal of Clinical Investigation
|September 1, 1994
PubMed

Insights

Shigella flexneri infection triggers peritoneal macrophages to release interleukin-1 (IL-1) during apoptosis. This early IL-1 release, before cell damage, suggests a role in initiating inflammation in epithelial tissues.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Peritoneal macrophages are key immune cells involved in host defense.
  • Shigella flexneri is a pathogen that invades epithelial cells and can trigger inflammatory responses.
  • Apoptosis is programmed cell death, a critical process in immune regulation.

Purpose of the Study:

  • To investigate the inflammatory cytokine release profile of peritoneal macrophages undergoing apoptosis induced by Shigella flexneri.
  • To determine if apoptosis in macrophages infected with Shigella flexneri leads to the release of specific cytokines like IL-1, IL-6, or TNF alpha.
  • To elucidate the mechanism and timing of IL-1 release during Shigella-induced macrophage apoptosis.

Main Methods:

  • Primary peritoneal macrophages were isolated and prestimulated.
  • Macrophages were infected with wild-type Shigella flexneri.
  • Cytokine levels (IL-1, IL-6, TNF alpha) in the supernatant were measured.
  • Cell integrity was assessed to correlate cytokine release with apoptosis.

Main Results:

  • Shigella flexneri infection induced apoptosis in peritoneal macrophages.
  • A rapid and significant release of interleukin-1 (IL-1) was observed from infected macrophages.
  • Neither IL-6 nor TNF alpha were released in significant amounts.
  • Both IL-1 alpha and mature IL-1 beta were detected, originating from presynthesized cytoplasmic pools.
  • IL-1 release occurred before the compromise of macrophage integrity.

Conclusions:

  • Bacteria-induced apoptosis of macrophages actively contributes to the inflammatory process.
  • The early release of IL-1 by dying macrophages plays a crucial role in initiating inflammatory responses in epithelial tissues during Shigella infection.

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