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Published ahead of print on March 25, 2004, doi:10.1165/rcmb.2004-0078OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 2, August 2004, 241-245

A more recent version of this article appeared on August 1, 2004
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Submitted on March 2, 2004
Revised on March 25, 2004

Expression of functional Toll-like receptor (TLR-)2 and TLR-4 on alveolar epithelial cells

Lynne Armstrong1*, Andrew R.L. Medford1, Kay M Uppington1, John Robertson2, Ian R Witherden3, Teresa D Tetley4, and Ann B Millar1

1 Lung Research Group, University of Bristol, Bristol, United Kingdom, 2 Department of Respiratory Medicine, Bristol Royal Infirmary, Bristol, United Kingdom, 3 Academic Renal Unit, University of Bristol, Bristol, United Kingdom, 4 Department of Respiratory Medicine, National Heart and Lung Institute, London, United Kingdom

* To whom correspondence should be addressed. E-mail: lynne.armstrong{at}bris.ac.uk.

The recognition of potentially harmful micro-organisms involves the specific recognition of pathogen-associated molecular patterns (PAMPs) and the family of Toll-like receptors (TLRs) are known to play a central role in this process. TLR-4 is the major recognition receptor for LPS, a component of gram negative bacterial cell walls, whereas TLR-2 responds to bacterial products from gram positive organisms. Although resident alveolar macrophages are the first line of defense against microbial attack, it is now understood that the alveolar epithelium also plays a pivotal role in the innate immunity of the lung. The purpose of the current study was to determine whether human primary type II alveolar epithelial cells (ATII) express functional TLR-2 and TLR-4 and how they my be regulated by inflammatory mediators. We have utilized RT-PCR and flow cytometry to determine basal and inducible expression on ATII. We have used highly purified preparations of the gram positive bacterial product lipoteichoic acid (LTA) and LPS to look at the functional consequences of TLR-2 and TLR-4 ligation respectively in terms of IL-8 release. We have shown that human primary ATII cells express mRNA and protein for both TLR-2 and TLR-4, which can be modulated by incubation with LPS and TNF. Furthermore, we have demonstrated that these receptors are functional. This suggests that ATII have the potential to contribute significantly to the host defence of the human alveolus against bacteria.




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