HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 288/5/G1048    most recent 00241.2004v2 00241.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Kohler, J. E. Articles by Alverdy, J. C. Search for Related Content PubMed PubMed Citation Articles by Kohler, J. E. Articles by Alverdy, J. C.

INFLAMMATION/IMMUNITY/MEDIATORS

Components of intestinal epithelial hypoxia activate the virulence circuitry of Pseudomonas

¹Departments of Surgery and ²Pathology, ³Clinical Microbiology Laboratories, ⁴Molecular Genomics and Cell Biology, and ⁵Biochemistry and Molecular Biology, University of Chicago, Chicago, Illinois

Submitted 1 June 2004 ; accepted in final form 23 October 2004

We have previously shown that a lethal virulence trait in Pseudomonas aeruginosa, the PA-I lectin, is expressed by bacteria within the intestinal lumen of surgically stressed mice. The aim of this study was to determine whether intestinal epithelial hypoxia, a common response to surgical stress, could activate PA-I expression. A fusion construct was generated to express green fluorescent protein downstream of the PA-I gene, serving as a stable reporter strain for PA-I expression in P. aeruginosa. Polarized Caco-2 monolayers were exposed to ambient hypoxia (0.1–0.3% O₂) for 1 h, with or without a recovery period of normoxia (21% O₂) for 2 h, and then inoculated with P. aeruginosa containing the PA-I reporter construct. Hypoxic Caco-2 monolayers caused a significant increase in PA-I promoter activity relative to normoxic monolayers (165% at 1 h; P < 0.001). Similar activation of PA-I was also induced by cell-free apical, but not basal, media from hypoxic Caco-2 monolayers. PA-I promoter activation was preferentially enhanced in bacterial cells that physically interacted with hypoxic epithelia. We conclude that the virulence circuitry of P. aeruginosa is activated by both soluble and contact-mediated elements of the intestinal epithelium during hypoxia and normoxic recovery.

epithelial cells; stress

This article has been cited by other articles:

				N. J. Patel, O. Zaborina, L. Wu, Y. Wang, D. J. Wolfgeher, V. Valuckaite, M. J. Ciancio, J. E. Kohler, O. Shevchenko, S. P. Colgan, et al. Recognition of intestinal epithelial HIF-1{alpha} activation by Pseudomonas aeruginosa Am J Physiol Gastrointest Liver Physiol, January 1, 2007; 292(1): G134 - G142. [Abstract] [Full Text] [PDF]