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Published ahead of print on December 4, 2003, doi:10.1165/rcmb.2003-0329OC

Am. J. Respir. Cell Mol. Biol., Volume 30, Number 6, June 2004, 777-783

A more recent version of this article appeared on June 1, 2004
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Submitted on September 5, 2003
Revised on December 3, 2003

Toll like receptors in normal and cystic fibrosis airway epithelial cells

Amanda Muir1, Grace Soong1, Sach Sokol1, Bharat Reddy1, Marisa Gomez1, Anna van Heeckeren2, and Alice Prince1*

1 Pediatrics, Columbia University, New York, NY, USA, 2 Pediatrics, Case Western Reserve University, Cleveland, OH, USA

* To whom correspondence should be addressed. E-mail: asp7{at}columbia.edu.

Toll like receptors (TLRs) mediate cellular responses to diverse microbial ligands. The distribution and function of TLRs in airway cells were studied to identify which are available to signal the presence of inhaled pathogens and to establish if differences in TLR expression are associated with the increased proinflammatory responses seen in cystic fibrosis. Isogenic, polarized CF and control bronchial epithelial cell lines, human airway cells in primary culture and cftr null and wild type mice were compared. TLRs 1-10, MD2, and MyD88 were expressed in CF and normal cells. Only TLR2 transcription was modestly increased in CF as compared with normal epithelial cells following bacterial stimulation. TLR2 was predominantly at the apical surface of airway cells and was mobilized to cell surface in response to bacteria. TLR4 was present in a more basolateral distribution in airway cells, but appeared to have a limited role in epithelial responses. LPS failed to activate NF-{kappa}B in these cells and TLR2 DN but not TLR4 DN mutants, inhibited activation by both Gram negative and Gram positive bacteria. Increased availability of TLR2 at the apical surfaces of CF epithelial cells is consistent with the increased proinflammatory responses seen in CF airways and suggests a selective participation of TLRs in the airway mucosa.




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Copyright © 2003 American Thoracic Society.