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Infection and Immunity, March 2000, p. 1289-1296, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Induction of Necrosis in Human Neutrophils by Shigella flexneri Requires Type III Secretion, IpaB and IpaC Invasins, and Actin Polymerization

Mathias François,1 Véronique Le Cabec,1 Marie-Ange Dupont,2 Philippe J. Sansonetti,3 and Isabelle Maridonneau-Parini1,*

Institut de Pharmacologie et de Biologie Structurale, CNRS UPR 9062,1 and Laboratoire de Biologie Moléculaire Eucaryote, CNRS UPR 9006,2 Toulouse, and Unité de Pathogénie Microbienne Moléculaire, Institut Pasteur, Paris,3 France

Received 24 September 1999/Returned for modification 29 October 1999/Accepted 6 December 1999

Infection by Shigella flexneri is characterized by infiltration of neutrophils in the intestinal mucosa and by a strong inflammatory reaction. Although neutrophils are constitutively programmed to die by apoptosis, we show that isolated human neutrophils undergo necrosis 2 h after infection with virulent S. flexneri strain M90T but not with the virulence plasmid-cured strain BS176. This was demonstrated by the release of azurophil granule proteins concomitant with the release of lactate dehydrogenase (LDH), disruption of the plasma membrane, and absence of DNA fragmentation. Mutants with the mxiD1 gene, coding for an essential component of the secretion type III machinery, or the genes coding for IpaB or IpaC invasins deleted were not cytotoxic. Neutrophil necrosis occurred independently of the bacterial ability to leave phagosomes, and it involved actin polymerization, as the addition of cytochalasin D after phagocytosis of Shigella inhibited the release of LDH. In conclusion, Shigella kills neutrophils by necrosis, a process characterized by the release of tissue-injurious granular proteins. This probably contributes to disruption of the epithelial barrier, leading to the dysentery observed in shigellosis and allowing Shigella to enter its host cells.

* Corresponding author. Mailing address: CNRS-IPBS, 205 Route de Narbonne, 31077 Toulouse, France. Phone: 33-561 14 54 58. Fax: 33-561 17 59 94. E-mail: maridono{at}ipbs.fr.

Infection and Immunity, March 2000, p. 1289-1296, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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