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Infect Immun. 1993 Sep;61(9):3625-35.

OmpC is involved in invasion of epithelial cells by Shigella flexneri.

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  • 1Unité de Pathogénie Microbienne Moléculaire, Institut National de la Santé et de la Recherche Médicale, U 199, Institut Pasteur, Paris, France.


Osmoregulation of the Shigella flexneri ompC gene and the role of OmpC in Shigella virulence have been investigated. OmpC was highly expressed when bacteria were grown in medium of either low or high osmolarity. This constitutive expression is in contrast with the regulation observed in Escherichia coli, in which the expression of OmpC is repressed at low osmolarity and induced at high osmolarity. In addition, the Shigella ompC gene was barely expressed by a delta ompB (delta ompR and delta envZ) mutant. We described in a previous report that such a mutant was severely impaired in virulence both in vitro and in vivo. Starting from this observation, and in order to assess which gene(s) regulated by ompR and envZ are involved in virulence, we constructed an S. flexneri delta ompC mutant. Three S. flexneri mutants, ompF'-lacZ, delta ompC, and delta ompB, were compared for virulence. The ompF'lacZ mutant behaved like the S. flexneri serotype 5 wild-type strain M90T in all in vitro and in vivo virulence tests. On the contrary, the delta ompB and delta ompC strains were considerably impaired in their virulence phenotypes. The ability of these two mutants to spread from cell to cell and to kill epithelial cells was severely affected. Consequently delta ompC, as previously described for delta ompB, was unable to elicit a positive Sereny test. The delta ompB mutant was restored to virulence by introducing a recombinant multicopy plasmid carrying the cloned E. coli ompC gene, indicating that a functional OmpC protein was necessary and sufficient to restore virulence to this mutant of S. flexneri.

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