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Published ahead of print on December 23, 2004, doi:10.1165/rcmb.2004-0196OC

Am. J. Respir. Cell Mol. Biol., Volume 32, Number 4, April 2005, 262-267

A more recent version of this article appeared on April 1, 2005
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Submitted on June 18, 2004
Revised on December 23, 2004

Primary Human Alveolar Type II Epithelial cell CCL20 (MIP-3{alpha})-induced dendritic cell migration

Andrew J Thorley1, Peter Goldstraw2, Alan Young3, and Teresa D Tetley1*

1 Lung Cell Biology, Imperial College, National Heart and Lung Institute, London, United Kingdom, 2 Department of Thoracic Surgery, Royal Brompton and Harefield NHS Trust, London, United Kingdom, 3 AstraZeneca, Loughborough, United Kingdom

* To whom correspondence should be addressed. E-mail: t.tetley{at}imperial.ac.uk.

Inhalation of antigenic matter stimulates rapid recruitment of dendritic cells (DC) into the lung. Recent studies propose that the chemokine CCL20 (MIP-3{alpha}) may play an important role in DC recruitment. We previously showed that primary human alveolar type II epithelial (ATII) cells are a rich source of chemokines and so hypothesised that the ATII cell produces CCL20 and might therefore be a key regulator of dendritic cell recruitment into the lung. Here, we show that primary human ATII cells, but not human alveolar macrophages, produce CCL20 both constitutively (403.5pg/ml ± 85.4; 24hours) and in response to endotoxin (lipopolysaccharide; LPS) exposure (1525.0pg/ml ± 169.4; 1µg/ml LPS; 24hours) in a time- and dose-dependent manner. In addition we show that peripheral blood monocyte-derived CD1a+ DCs migrate in response to conditioned media from ATII cells but not that from alveolar macrophages; DC migration was significantly correlated with the amount of CCL20 (r2>0.9; p<0.05) detected in the media but not with any other chemokine measured. We therefore conclude that the alveolar epithelium is an important source of CCL20 in the lung and that the ATII cell may play a critical role in controlling the movement of DCs through the lung both under normal and inflammatory conditions.




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