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Fourteen-Membered Ring Macrolides Inhibit Vascular Cell Adhesion Molecule-1 Messenger RNA Induction Preventing Neutrophil-Induced Lung Injury and Fibrosis in Bleomycin-Challenged Mice*

Arata Azuma, MD, PhD; Yingji Li; Jiro Usuki, MD; Akinori Aoyama; Ttsuji Enomoto; Shoji Kudoh, MD
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*From the Fourth Department of Internal Medicine, Nippon Medical School, Bunkyo-ku, Tokyo, Japan.

Correspondence to: Arata Azuma, MD, PhD, Fourth Department of Internal Medicine, Nippon Medical School, 1–1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan; e-mail: azuma/med4@nms.ac.jp



Chest. 2001;120(1_suppl):S20-S22. doi:10.1378/chest.120.1_suppl.S20-a
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It has been reported14 that neutrophils and the injurious substances associated with them play an important role in the progression of lung fibrosis induced by bleomycin (BLM). We have reported5 further that E-selectin plays an essential role in the neutrophil adhesion to endothelial cells, the subsequent migration of neutrophils into lung tissue, and the progression of lung fibrosis. A new structural macrolide, macrosphelide-A, which is an inhibitor for sialyl-LeX-dependent adhesion of HL60 cells against vascular endothelial cells, successfully inhibits BLM-induced lung fibrosis.6 Fourteen-membered ring macrolides (14-MRMLs) have been reported7 to improve the survival times of patients with diffuse panbronchiolitis owing to several anti-inflammatory mechanisms. In the present study, we investigated the mechanisms of the preventive effect of 14-MRML (ie, erythromycin [EM], clarithromycin [CAM], and roxithromycin [RXM]) in mice with BLM-induced lung fibrosis.

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