Published ahead of print on September 15, 2005, doi:10.1165/rcmb.2005-0236OC Am. J. Respir. Cell Mol. Biol., Volume 33, Number 6, December 2005, 565-573 A more recent version of this article appeared on December 1, 2005
Submitted on June 29, 2005 Involvement of Discoidin Domain Receptor 1 in the Deterioration of Pulmonary SarcoidosisWataru Matsuyama1*,1 Respiratory and Stress Care Center, Division of Respiratory Medicine, Kagoshima University Hospital, Kagoshima, Japan * To whom correspondence should be addressed. E-mail: vega{at}xa2.so-net.ne.jp.
The prognosis of sarcoidosis with pulmonary infiltrates differs in each case and several cytokines are reported to contribute to its deterioration. However, the detailed mechanism has not been fully elucidated. Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase activated by collagen and associated with cytokine productions from inflammatory cells. We previously reported the functional expression of DDR1 on CD14 positive bronchoalveolar lavage fluid (BALF) cells in vivo. In this study, we hypothesized that DDR1 might be associated with the deterioration of pulmonary sarcoidosis, and investigated 33 sarcoidosis patients with pulmonary infiltrates, prospectively. We found that deteriorated pulmonary sarcoidosis patients showed significantly higher DDR1 expression amount in CD14 positive BALF cells predominant with DDR1b isoforms. Activation of DDR1 induced monocyte chemoattractant protein-1 (MCP-1) and matrix metalloproteinase-9 (MMP-9) production via p38 mitogen activated protein kinase dependent manner from CD14 positive BALF cells of deteriorated sarcoidosis patients. DDR1 activation also induced NF-
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B nuclear translocation in CD14 positive BALF cells of deteriorated pulmonary sarcoidosis patients. The inhibitor of NF-
