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Infect. Immun. doi:10.1128/IAI.00082-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Helicobacter pylori chemotaxis modulates inflammation and gastric-epithelium interactions in infected mice

Department of Environmental Toxicology, University of California at Santa Cruz, Santa Cruz, CA 95064; Department of Pathology, University of South Alabama College of Medicine, Mobile, AL, 36688 USA; Department of Microbiology and Immunology, Louisiana State University Health Science Center, Shreveport, LA, 71130 USA

^* To whom correspondence should be addressed. Email: ottemann{at}ucsc.edu.

	Abstract

The ulcer-causing pathogen Helicobacter pylori uses directed motility, or chemotaxis, to both colonize the stomach and promote disease development. Previous work showed that mutants lacking the TlpB chemoreceptor, one of the receptors predicted to drive chemotaxis, led to less inflammation in the gerbil stomach than did wild type. Here we expanded these findings and examined the effects on inflammation of completely nonchemotactic mutants and mutants lacking each chemoreceptor. Of note, all mutants colonized mice to the same levels as did wild-type H. pylori. Infection by completely nonchemotactic mutants (cheW or cheY) resulted in significantly less inflammation after both three and six months of infection. Mutants lacking either the TlpA or TlpB H. pylori chemotaxis receptors also had alterations in inflammation severity, while mutants lacking either of the other two chemoreceptors (TlpC and HylB) behaved like wild type. Fully nonchemotactic and chemoreceptor mutants adhered to cultured gastric epithelial cells, and caused similar cellular release of the chemokine IL-8 in vitro as did wild type. The situation appeared different in the stomach. Using silver-stained histological sections, we found that nonchemotactic cheY or cheW mutants were less likely than wild type to be intimately associated with the cells of the gastric mucosa, although there was not a strict correlation between intimate association and inflammation. Because others have shown that in vivo adherence promotes inflammation, we propose a model in which H. pylori uses chemotaxis to guide it to a productive interaction with the stomach epithelium.

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