Attenuation of lung inflammation and fibrosis in CD69-deficient mice after intratracheal bleomycinReport as inadecuate

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Respiratory Research

, 12:131

First Online: 01 December 2011Received: 27 June 2011Accepted: 05 October 2011


BackgroundCluster of differentiation 69 CD69, an early activation marker antigen on T and B cells, is also expressed on activated macrophages and neutrophils, suggesting that CD69 may play a role in inflammatory diseases. To determine the effect of CD69 deficiency on bleomycinBLM-induced lung injury, we evaluated the inflammatory response following intratracheal BLM administration and the subsequent fibrotic changes in wild type WT and CD69-deficient CD69 mice.

MethodsThe mice received a single dose of 3 mg-kg body weight of BLM and were sacrificed at 7 or 14 days post-instillation dpi. Lung inflammation in the acute phase 7 dpi was investigated by differential cell counts and cytokine array analyses of bronchoalveolar lavage fluid. In addition, lung fibrotic changes were evaluated at 14 dpi by histopathology and collagen assays. We also used reverse transcription polymerase chain reaction to measure the mRNA expression level of transforming growth factor β1 TGF-β1 in the lungs of BLM-treated mice.

ResultsCD69 mice exhibited less lung damage than WT mice, as shown by reductions in the following indices: 1 loss of body weight, 2 wet-dry ratio of lung, 3 cytokine levels in BALF, 4 histological evidence of lung injury, 5 lung collagen deposition, and 6 TGF-β1 mRNA expression in the lung.

ConclusionThe present study clearly demonstrates that CD69 plays an important role in the progression of lung injury induced by BLM.

Keywordscluster of differentiation 69 lung inflammation pulmonary fibrosis bleomycin Electronic supplementary materialThe online version of this article doi:10.1186-1465-9921-12-131 contains supplementary material, which is available to authorized users.

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Author: Keita Yamauchi - Yoshitoshi Kasuya - Fuminobu Kuroda - Kensuke Tanaka - Junichi Tsuyusaki - Shunsuke Ishizaki - Hirofumi Ma


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