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J. Biol. Chem., Vol. 280, Issue 44, 36714-36718, November 4, 2005

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Nod1 Participates in the Innate Immune Response to Pseudomonas aeruginosa^*

Leonardo H. Travassos12, Leticia A. M. Carneiro23, Stephen E. Girardin¶4, Ivo G. Boneca||5, Ramon Lemos6, Marcelo T. Bozza, Regina C. P. Domingues, Anthony J. Coyle**, John Bertin**, Dana J. Philpott7, and Maria Cristina Plotkowski7

From the Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ Cep. 21.941 590, Brazil, Faculdade de Ciências Médicas, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ Cep. 20551-030, Brazil, ^¶Unité de Pathogénie Microbienne Moleculaire, ^||Unité de Pathogénie Bacteriénne des Muqueuses, and Groupe d'Immunité Innée et Signalisation, Institut Pasteur, 75724 Paris Cedex 15, France, and ^**Millenium Pharmaceuticals, Cambridge, Massachusetts 02139

The mammalian innate immune system recognizes pathogen-associated molecular patterns through pathogen recognition receptors. Nod1 has been described recently as a cytosolic receptor that detects specifically diaminopimelate-containing muropeptides from Gram-negative bacteria peptidoglycan. In the present study we investigated the potential role of Nod1 in the innate immune response against the opportunistic pathogen Pseudomonas aeruginosa. We demonstrate that Nod1 detects the P. aeruginosa peptidoglycan leading to NF-B activation and that this activity is diminished in epithelial cells expressing a dominant-negative Nod1 construct or in mouse embryonic fibroblasts from Nod1 knock-out mice infected with P. aeruginosa. Finally, we demonstrate that the cytokine secretion kinetics and bacterial killing are altered in Nod1-deficient cells infected with P. aeruginosa in the early stages of infection.

Received for publication, February 11, 2005 , and in revised form, August 18, 2005.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

² These authors contributed equally to this work.

³ Supported by a studentship from the National Council of Technological and Scientific Development (CNPq)/Brazil.

⁴ Supported by a grant from Danone Vitapole, Paris, France and by the Institut Pasteur, Paris, France.

⁵ Supported by Fundação para Ciencia e Tecnologia, Portugal, and the Institut Pasteur, Paris, France.

⁶ Supported by a studentship from CAPES/MEC, Brazil.

⁷ These authors share senior authorship.

¹ Supported by a studentship from Coordenacão de Aperfeiçoamento de Pessoal de Nîvel Superior/Ministêrio de Educaçao (CAPES/MEC), Brazil. To whom correspondence should be addressed: Universidade Federal do Rio de Janeiro, Centro de Ciências da Saúde (Bloco I), Instituto de Microbiologia Prof. Paulo de Góes Centro de Cidade Universitária, Ilha do Fundão, Rio de Janeiro, RJ Cep. 21.941 590. Tel.: 55-21-25626748; Fax: 55-21-25608344; E-mail: lhtravassos{at}ufrj.br.

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