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Chemokines in bronchiolar epithelium in the development of chronic obstructive pulmonary disease.

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/17090

Title: Chemokines in bronchiolar epithelium in the development of chronic obstructive pulmonary disease.
Authors: Fuke, Satoshi Browse this author
Betsuyaku, Tomoko Browse this author →KAKEN DB
Nasuhara, Yasuyuki Browse this author →KAKEN DB
Morikawa, Toshiaki Browse this author
Katoh, Hiroyuki Browse this author
Nishimura, Masaharu Browse this author →KAKEN DB
Issue Date: Oct-2004
Publisher: American Thoracic Society
Journal Title: American Journal of Respiratory Cell and Molecular Biology
Volume: 31
Issue: 4
Start Page: 405
End Page: 412
Publisher DOI: 10.1165/rcmb.2004-0131OC
PMID: 15220136
Abstract: The inflammatory chemokines interleukin-8, macrophage inflammatory protein-1, and monocyte chemoattractant protein-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 and explored the relationship with early-stage COPD. Only in bronchiolar epithelial cells were interleukin-8, macrophage inflammatory protein-1, and monocyte chemoattractant protein-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. Complementary DNA (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 laser-capture microdissection, combined with reverse transcriptase–polymerase chain reaction and cDNA microarrays, to investigate functional profiles of individual structural and inflammatory cells in human lungs.
Relation: http://ajrcmb.atsjournals.org/
Type: article
URI: http://hdl.handle.net/2115/17090
Appears in Collections:北海道大学病院 (Hokkaido University Hospital) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 別役 智子

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