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Article
Nature Immunology  5, 1166 - 1174 (2004)
Published online: 17 October 2004; | doi:10.1038/ni1131

Nod1 responds to peptidoglycan delivered by the Helicobacter pylori cag pathogenicity island

Jérôme Viala1, Catherine Chaput2, Ivo G Boneca2, Ana Cardona3, Stephen E Girardin4, Anthony P Moran5, Rafika Athman1, Sylvie Mémet6, Michel R Huerre3, Anthony J Coyle7, Peter S DiStefano7, Philippe J Sansonetti4, Agnès Labigne2, John Bertin7, Dana J Philpott1, 6 & Richard L Ferrero2, 8

1  Groupe d'Immunité Innée et Signalisation, Institut National de la Santé et de la Recherche Médicale U389, Institut Pasteur, Paris, France.

2  Unité de Pathogénie Bactérienne des Muqueuses, Institut National de la Santé et de la Recherche Médicale U389, Institut Pasteur, Paris, France.

3  Unité de Recherche et d'Expertise Histotechnologie et Pathologie, Institut National de la Santé et de la Recherche Médicale U389, Institut Pasteur, Paris, France.

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

5  Department of Microbiology, National University of Ireland, Galway, Ireland.

6  Unité de Biologie Moléculaire de l'Expression Génique, Institut Pasteur, Paris, France.

7  Millenium Pharmaceuticals, Cambridge, Massachusetts, USA.

8  Present address: Department of Microbiology, Monash University, Clayton, 3800 Victoria, Australia.

Correspondence should be addressed to Richard L Ferrero Richard.Ferrero@med.monash.edu.au
Epithelial cells can respond to conserved bacterial products that are internalized after either bacterial invasion or liposome treatment of cells. We report here that the noninvasive Gram-negative pathogen Helicobacter pylori was recognized by epithelial cells via Nod1, an intracellular pathogen-recognition molecule with specificity for Gram-negative peptidoglycan. Nod1 detection of H. pylori depended on the delivery of peptidoglycan to host cells by a bacterial type IV secretion system, encoded by the H. pylori cag pathogenicity island. Consistent with involvement of Nod1 in host defense, Nod1-deficient mice were more susceptible to infection by cag pathogenicity island−positive H. pylori than were wild-type mice. We propose that sensing of H. pylori by Nod1 represents a model for host recognition of noninvasive pathogens.

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Nature Immunology
ISSN: 1529-2908
EISSN: 1529-2916
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