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Published ahead of print on November 11, 2005, doi:10.1165/rcmb.2005-0191OC
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American Journal of Respiratory Cell and Molecular Biology. Vol. 34, pp. 348-354, 2006
© 2006 American Thoracic Society
DOI: 10.1165/rcmb.2005-0191OC

T Cell Chemotaxis and Chemokine Release after Staphylococcus aureus Interaction with Polarized Airway Epithelium

Sandie Escotte, Denise Al Alam, Richard Le Naour, Edith Puchelle, Moncef Guenounou and Sophie C. Gangloff

Laboratoire d'Immuno-Pharmacologie Cellulaire et Moléculaire, EA3796, Université de Reims Champagne Ardennes, IFR53; and INSERM UMRS 514, IFR 53, Reims, France

Correspondence and requests for reprints should be addressed to Prof. S. C. Gangloff, Laboratoire d'Immuno-pharmacologie cellulaire et moléculaire, EA3796-IFR53, 1 Avenue du Maréchal Juin, 51100 Reims, France. 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 S. 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 toward apical supernatant. Our data strongly suggest that S. aureus interaction with airway epithelium contributes to specific migration of T cells to inflamed sites.

Key Words: airway epithelial cells • chemokines • chemotaxis • Staphylococcus aureus • T lymphocytes




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