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Published ahead of print on November 11, 2005, doi:10.1165/rcmb.2005-0191OC

Am. J. Respir. Cell Mol. Biol., Volume 34, Number 3, March 2006, 348-354

A more recent version of this article appeared on March 1, 2006
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Submitted on May 18, 2005
Revised on November 11, 2005

T Cell Chemotaxis and Chemokine Release After S.aureus Interaction with Polarized Airway Epithelium

Sandie Escotte1, Denise Al Alam1, Richard Le Naour1, Edith Puchelle2, Moncef Guenounou1, and Sophie C Gangloff1*

1 Laboratoire d'Immuno-Pharmacologie Cellulaire et Moleculaire, EA3796, Universite of Reims Champagne Ardennes, IFR53, Reims, France, 2 INSERM UMRS 514, Reims, France

* To whom correspondence should be addressed. E-mail: Sophie.gangloff {at}univ-reims.fr.

In response to bacterial infection, airway epithelium releases inflammatory mediators including cytokines and chemokines that lead to immune cell efflux and could stimulate the adaptive T cell immune response. The aim of our study was to analyze, in a double chamber culture, the chemokine changes in response to Staphylococcus aureus and their consequences for T cells. Our data show that Staphylococcus aureus stimulates basolateral and apical release of IL-8 and eotaxin by airway epithelial cells. We also observed increased chemokine receptor expression on CD8+ and CD4+ T cells and enhanced chemotaxis of CD4+ T cells towards apical supernatant. Our data strongly suggest that Staphylococcus aureus interaction with airway epithelium contributes to specific migration of T cells to inflamed sites.




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