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Institut Pasteur, Unité des interactions Bactéries cellules, Paris, F-75015; France, INSERM, U604, Paris, F-75015; France, INRA, USC2020, Paris, F-75015; France, Service des Maladies infectieuses et tropicales, Université Paris 5, Hôpital Necker-Enfants malades. 75015 Paris. France, Unité de Biologie des Bactéries pathogènes à Gram-positif Institut Pasteur, 75724 Paris Cedex 15. France
* To whom correspondence should be addressed. Email: hbierne{at}pasteur.fr.
| Abstract |
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The food-borne pathogen Listeria monocytogenes is adapted to a diversity of environments, such as soil, food, body fluids and the cytosol of eukaryotic cells. The transition between saprophytic and pathogenic life is mediated through complex regulatory pathways that modulate expression of virulence factors. Here we examined expression of inlJ, a recently identified gene of the LPXTG-internalin family, involved in pathogenesis. We show that inlJ expression is neither controlled by the major listerial regulator of virulence genes PrfA, nor by AxyR, an AraC putative regulator encoded by a gene adjacent to inlJ and divergently transcribed. The InlJ protein is not produced by bacteria grown in vitro in BHI medium or replicating in the cytosol of tissue-cultured cells. In contrast, it is efficiently produced and localized at the surface of bacteria present in the liver and blood of infected animals. Strikingly, expression of inlJ by a heterologous promoter in L. monocytogenes or L. innocua promotes bacterial adherence to human cells in vitro. Taken together, these results strongly suggest that InlJ acts as a novel L. monocytogenes sortase-anchored adhesin specifically expressed during host infection.
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
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| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
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