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Published ahead of print on June 25, 2004, doi:10.1165/rcmb.2004-0131OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 4, October 2004, 405-412

A more recent version of this article appeared on October 1, 2004
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Submitted on April 26, 2004
Revised on June 25, 2004

Chemokines in Bronchiolar Epithelium in the Development of Chronic Obstructive Pulmonary Disease

Satoshi Fuke1, Tomoko Betsuyaku1*, Yasuyuki Nasuhara1, Toshiaki Morikawa2, Hiroyuki Katoh2, and Masaharu Nishimura1

1 First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan, 2 Second Department of Surgery, Hokkaido University School of Medicine, Sapporo, Japan

* To whom correspondence should be addressed. E-mail: bytomoko{at}med.hokudai.ac.jp.

The inflammatory chemokines interleukin-8 (IL-8), macrophage inflammatory protein-1 alpha (MIP-1 alpha) and monocyte chemoattractant protein-1 (MCP-1), are reportedly involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Although bronchiolar epithelial cells and macrophages are known to be the cellular sources, the relative contribution of each cell type remains to be elucidated. In the present study, we first quantified cytokine mRNA in human bronchiolar epithelial cells and macrophages obtained using laser capture microdissection (LCM) and explored the relationship with early-stage COPD. Only in bronchiolar epithelial cells were IL-8, MIP-1 alpha and MCP-1 mRNA levels higher in smokers with airflow limitation and/or emphysema than those in never-smokers or smokers without either airflow limitation or emphysema. No difference was observed in macrophages. cDNA array further revealed the overexpression of CC chemokine receptor 2 in bronchiolar epithelial cells from smokers with airflow limitation and/or emphysema. This study supports the role of bronchiolar epithelium as the source of increased inflammatory chemokine levels in the early development of COPD and also demonstrates the potential use of LCM combined with reverse transcriptase-polymerase chain reaction and cDNA microarrays to investigate functional profiles of individual structural and inflammatory cells in human lungs.




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