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Originally published In Press as doi:10.1074/jbc.M203239200 on May 2, 2002

J. Biol. Chem., Vol. 277, Issue 28, 25133-25142, July 12, 2002
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Regulation of mRNA Expression in Macrophages after Yersinia enterocolitica Infection
ROLE OF DIFFERENT Yop EFFECTORS*

Nathalie SauvonnetDagger §, Bérengère Pradet-Balade§||, Jose A. Garcia-Sanz||, and Guy R. CornelisDagger **Dagger Dagger

From the Dagger  Microbial Pathogenesis Unit, Christian de Duve Institute of Cellular Pathology and Université Catholique de Louvain, B-1200 Brussels, Belgium, || Department of Immunology and Oncology, Centro Nacional de Biotecnología, E-28049 Madrid, Spain, and ** Biozentrum der Universität Basel, CH-4056 Basel, Switzerland

The Yop virulon, which comprises a complete type III secretion system and secreted proteins, allows bacteria from the genus Yersinia to resist the nonspecific immune response of the host. This virulon, which is encoded by a plasmid called pYV in Yersinia enterocolitica, enables extracellular bacteria to inject six Yop effectors (YopE, -H, -T, -O, -P, -M) into the host cell. To investigate the role of YopP, YopM, and the other pYV-encoded factors on the expression of the host cell genes, we characterized the transcriptome alterations in infected mouse macrophages using the microarray technique. PU5-1.8 macrophages were infected either with an avirulent (pYV-), a wild type (pYV+), or two knockout (yopP- and yopM-) mutants of Y. enterocolitica. Expression alterations in response to Y. enterocolitica infection were monitored for 6657 genes. Among those, 857 genes were affected, 339 of which were specifically regulated by the action of the Yop virulon. Further analysis of those 339 genes allowed identification of specific targets of YopP, YopM, or the other pYV-encoded factors. According to these results, the main action of the Yop virulon is to counteract the host cell pro-inflammatory response to the infection. YopP participates to this inhibition, whereas another pYV-encoded factor appears to also be involved in this down-regulation. Besides, YopM was found to induce the regulation of genes involved in cell cycle and cell growth, revealing for the first time an in vitro effect for YopM. In addition to YopM, other pYV factors distinct from YopP affected the expression of genes involved in cycling. In conclusion, these results provide new insight into the mechanisms of Yersinia pathogenicity by identifying the changes in host genes expression after infection and highlight the concerted actions of the different Yop effectors.

* This work was supported in part by a Training and Mobility of Researchers Program of the European Community (EU-TMR) Network grant (Contract ERBFMRXCT980197) (to J. A. G.-S.), Belgian Fonds National de la Recherche Scientifique Médicale (Convention 3.4595.97), and the Direction Générale de la Recherche Scientifique-Communauté Française de Belgique (Action de Recherche Concertée 94/99-172) (to G. C.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ These authors contributed equally to this work.

A Marie Curie fellow of the European Community (Contract QLK2-CT-1999-51051). Present address: Unité de Biologie des Interactions Cellulaires, Institut Pasteur, 75015 Paris, France.

Dagger Dagger To whom correspondence should be addressed: Biozentrum der Universität Basel, Klingelbergstrasse 50-70, CH-4056 Basel, Switzerland. Tel.: 41-61-267-21-10; Fax: 41-61-267-21-18; E-mail address: guy.cornelis@unibas.ch.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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