T cell chemotaxis and chemokine release after Staphylococcus aureus interaction with polarized airway epithelium

Am J Respir Cell Mol Biol. 2006 Mar;34(3):348-54. doi: 10.1165/rcmb.2005-0191OC. Epub 2005 Nov 11.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD4-Positive T-Lymphocytes / physiology
  • CD8-Positive T-Lymphocytes / physiology
  • Cell Polarity
  • Cells, Cultured
  • Chemokine CCL11
  • Chemokines / metabolism*
  • Chemokines, CC / metabolism
  • Chemotaxis, Leukocyte*
  • Epithelial Cells / metabolism
  • Epithelial Cells / microbiology*
  • Humans
  • Interleukin-8 / metabolism
  • Receptors, Chemokine / metabolism
  • Respiratory Mucosa / immunology
  • Respiratory Mucosa / metabolism
  • Respiratory Mucosa / microbiology*
  • Staphylococcus aureus / physiology*
  • T-Lymphocytes / physiology*
  • Trachea / cytology

Substances

  • CCL11 protein, human
  • Chemokine CCL11
  • Chemokines
  • Chemokines, CC
  • Interleukin-8
  • Receptors, Chemokine