AEM
Home Help [Feedback] [For Subscribers] [Archive] [Search] --
AEM Accepts, published online ahead of print on 11 January 2008
This Article
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
AEM.01507-07v1
74/5/1583    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Google Scholar
Right arrow Articles by Reid, A. N.
Right arrow Articles by Stintzi, A.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reid, A. N.
Right arrow Articles by Stintzi, A.
Agricola
Right arrow Articles by Reid, A. N.
Right arrow Articles by Stintzi, A.
Appl. Environ. Microbiol. doi:10.1128/AEM.01507-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Identification of Campylobacter jejuni genes involved in the response to acidic pH and stomach transit

Anne N. Reid, Reenu Pandey, Kiran Palyada, Hemant Naikare, and Alain Stintzi*

Ottawa Institute of Systems Biology, Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, K1H 8M5, Canada; Department of Veterinary Pathobiology, Oklahoma State University, Stillwater, OK, 74078, USA

* To whom correspondence should be addressed. Email: astintzi{at}uottawa.ca.


   Abstract

Campylobacter jejuni causes food- and water-borne gastroenteritis, and as such must survive passage through the stomach in order to reach the gastrointestinal tract. While little is known about how C. jejuni survives transit through the stomach, its low infectious dose suggests it is well equipped to sense and respond to acid shock. In this study, the transcriptional profile of C. jejuni NCTC 11168 was obtained after exposure to in vitro and in vivo (piglet stomach) acid shock. The observed down-regulation of genes encoding ribosomal proteins likely reflects the need to reshuffle energy towards the expression of components required for survival. Acid shock also caused C. jejuni to up-regulate genes involved in stress responses. These included heat shock genes, as well as genes involved in the response to oxidative and nitrosative stress. A role for the chaperone, clpB, in acid resistance was confirmed in vitro. Some genes showed expression patterns that were markedly different in vivo and in vitro, which likely reflects the complexity of the in vivo environment. For instance, transit through the stomach was characterized by up-regulation of genes whose products are involved in the use of nitrite as a terminal electron acceptor and down-regulation of genes involved in capsular polysaccharide expression. In conclusion, this study has enabled us to understand how C. jejuni modulates gene expression in response to acid shock in vitro, and to correlate this with gene expression profiles of C. jejuni as it transits through the host stomach.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] --
J. Bacteriol. Microbiol. Mol. Biol. Rev. Eukaryot. Cell All ASM Journals

Copyright © 2008 by the American Society for Microbiology. All rights reserved.