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Published ahead of print on December 23, 2004, doi:10.1165/rcmb.2004-0196OC
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American Journal of Respiratory Cell and Molecular Biology. Vol. 32, pp. 262-267, 2005
© 2005 American Thoracic Society
DOI: 10.1165/rcmb.2004-0196OC

Primary Human Alveolar Type II Epithelial Cell CCL20 (Macrophage Inflammatory Protein-3{alpha})–Induced Dendritic Cell Migration

Andrew J. Thorley, Peter Goldstraw, Alan Young and Teresa D. Tetley

Lung Cell Biology, National Heart and Lung Institute, Imperial College; Department of Thoracic Surgery, Royal Brompton and Harefield NHS Trust, London; and AstraZeneca R&D, Loughborough, United Kingdom

Correspondence and requests for reprints should be addressed to T. D. Tetley, Lung Cell Biology, National Heart & Lung Institute, Dovehouse Street, London SW3 6LY, UK. E-mail: t.tetley{at}imperial.ac.uk

Inhalation of antigenic matter stimulates rapid recruitment of dendritic cells (DCs) into the lung. Recent studies propose that the chemokine CCL20 (macrophage inflammatory protein-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 hypothesized that the ATII cell produces CCL20 and might therefore be a key regulator of DC recruitment into the lung. Here, we show that primary human ATII cells, but not human alveolar macrophages, produce CCL20 both constitutively (403.5 ± 85.4 pg/ml; 24 h) and in response to endotoxin (lipopolysaccharide) exposure (1,525.0 ± 169.4 pg/ml; 1 µg/ml lipopolysaccharide; 24 h) 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 those 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.

Key Words: dendritic cell • alveolar epithelium • chemokine




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