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Original Research: COPD |

Antiendothelial Cell Antibodies in Patients With COPD

Masato Karayama, MD; Naoki Inui, MD, PhD; Takafumi Suda, MD, PhD; Yutaro Nakamura, MD, PhD; Hirotoshi Nakamura, MD, PhD; Kingo Chida, MD, PhD
Author and Funding Information

From the Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Correspondence to: Naoki Inui, MD, PhD, 1-20-1 Handayama, Hamamatsu, Japan 431-3192; e-mail: inui@hama-med.ac.jp


Funding/Support: This study was supported in part by a grant to the Diffuse Lung Diseases Research Group from the Japanese Ministry of Health, Labour and Welfare.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(6):1303-1308. doi:10.1378/chest.10-0863
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Background:  Circulating antiendothelial cell antibodies (AECA) bind to endothelial antigens and induce endothelial cell damage. These antibodies have been detected in patients with collagen vascular diseases and systemic vasculitis. Recently, autoimmune mechanisms and vascular involvement have attracted attention in COPD. This study aimed to investigate the expression of AECA in patients with COPD.

Methods:  A total of 116 patients with COPD, whose condition was established based on the Global Initiative for Chronic Obstructive Lung Disease criteria, were evaluated. Serum samples were examined for AECA by a cellular enzyme-linked immunosorbent assay using human umbilical vein endothelial cells. In addition, 157 subjects without any clinical or radiologic evidence of COPD or pulmonary disease served as a reference population.

Results:  The patients with COPD exhibited significantly higher serum AECA concentrations than subjects in the reference population. The expression of AECA was significantly elevated in the patients with COPD, even when compared with that in smokers among the reference population who had similar smoking habits to the patients with COPD but normal spirometry.

Conclusions:  These findings suggest that an autoimmune component associated with endothelial cell damage is possibly involved in COPD.

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