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Research Article Free access | 10.1172/JCI117452

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

A Zychlinsky, C Fitting, J M Cavaillon, and P J Sansonetti

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

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

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

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

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Published September 1, 1994 - More info

Published in Volume 94, Issue 3 on September 1, 1994
J Clin Invest. 1994;94(3):1328–1332. https://doi.org/10.1172/JCI117452.
© 1994 The American Society for Clinical Investigation
Published September 1, 1994 - Version history
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Abstract

Peritoneal macrophages undergoing apoptosis induced by Shigella flexneri infection release the inflammatory cytokine interleukin 1 (IL-1), but not IL-6 or tumor necrosis factor alpha (TNF alpha). Wild type shigella causes a very fast and significant release of IL-1 from prestimulated peritoneal macrophages, before the cell's integrity is compromised. Both IL-1 alpha and IL-1 beta are released, IL-1 beta in its mature processed form. IL-1 is released from presynthesized cytoplasmic pools. These results demonstrate that bacteria-induced apoptosis of macrophages may play an active role in vivo by releasing IL-1, which in turn mediates an early inflammatory response in epithelial tissues.

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