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Infection and Immunity, February 2008, p. 551-561, Vol. 76, No. 2
0019-9567/08/$08.00+0     doi:10.1128/IAI.01107-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

NF-{kappa}B Activation during Acute Helicobacter pylori Infection in Mice{triangledown}

Richard L. Ferrero,1* Patrick Avé,2 Delphine Ndiaye,3 Jean-Christophe Bambou,1,{ddagger} Michel R. Huerre,2 Dana J. Philpott,4,§ and Sylvie Mémet3*

Unité de Pathogénie Bactérienne des Muqueuses,1 Unité de Recherche et d'Expertise Histotechnologie et Pathologie,2 Unité de Biologie Moléculaire de l'Expression Génique,3 Groupe d'Immunité Innée et Signalisation, Institut Pasteur, 25-28 rue du Dr Roux, Paris 75724, France4

Received 9 August 2007/ Returned for modification 17 September 2007/ Accepted 27 November 2007

Nuclear factor {kappa}B (NF-{kappa}B) plays a key regulatory role in host cell responses to Helicobacter pylori infection in humans. Although mice are routinely used as a model to study H. pylori pathogenesis, the role of NF-{kappa}B in murine cell responses to helicobacters has not been studied in detail. We thus investigated the abilities of different Helicobacter isolates to induce NF-{kappa}B-dependent responses in murine gastric epithelial cells (GECs) and in transgenic mice harboring an NF-{kappa}B-responsive lacZ reporter gene. H. pylori and Helicobacter felis strains up-regulated the synthesis in mouse GECs of the NF-{kappa}B-dependent chemokines KC (CXCL1) and MIP-2 (CXCL2). These responses were cag pathogenicity island (cagPAI) independent and could be abolished by pretreatment with a pharmacological inhibitor of NF-{kappa}B. Consistent with the in vitro data, experimental Helicobacter infection of transgenic mice resulted in increased numbers of GECs with nuclear β-galactosidase activity, which is indicative of specific NF-{kappa}B activation. The numbers of β-galactosidase-positive cells in mice were significantly increased at day 1 postinoculation with wild-type H. pylori strains harboring or not harboring a functional cagPAI, compared to naive animals (P = 0.007 and P = 0.04, respectively). Strikingly, however, no differences were observed in the levels of gastric NF-{kappa}B activation at day 1 postinoculation with H. felis or at day 30 or 135 postinoculation with H. pylori. This work demonstrates for the first time the induction of NF-{kappa}B activation within gastric mucosal cells during acute H. pylori infection. Furthermore, the data suggest that helicobacters may be able to regulate NF-{kappa}B signaling during chronic infection.

* Corresponding author. Present address for Richard L. Ferrero: Department of Microbiology, Monash University, Building 53, Wellington Road, Clayton, VIC 3800, Australia. Phone: (61) 3 9905 4842. Fax: (61) 3 9905 4811. E-mail: Richard.Ferrero{at}med.monash.edu.au. Present address for Sylvie Mémet: Unité de Mycologie Moléculaire, CNRS URA3012, Institut Pasteur, 25 rue du Docteur Roux, Paris 75724, France. Phone: (33) 1 40 61 32 55. Fax: (33) 1 45 68 84 20. E-mail: symemet{at}pasteur.fr

{triangledown} Published ahead of print on 10 December 2007.

Editor: B. A. McCormick

{ddagger} Present address: INRA Unité de Recherches Zootechniques, Guadeloupe, France.

§ Present address: Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada.

Infection and Immunity, February 2008, p. 551-561, Vol. 76, No. 2
0019-9567/08/$08.00+0     doi:10.1128/IAI.01107-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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