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肺纤维化模型 CD69 敲除小鼠肺组织炎症和纤维化的减轻。

Attenuation of lung inflammation and fibrosis in CD69-deficient mice after intratracheal bleomycin.

机构信息

Department of Respirology, Graduate School of Medicine, Chiba University, Chiba, Japan.

出版信息

Respir Res. 2011 Oct 5;12(1):131. doi: 10.1186/1465-9921-12-131.

DOI:10.1186/1465-9921-12-131
PMID:21970554
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3198935/
Abstract

BACKGROUND

Cluster 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 bleomycin(BLM)-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.

METHODS

The 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.

RESULTS

CD69-/- 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.

CONCLUSION

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

摘要

背景

分化群 69（CD69）是 T 和 B 细胞上的早期激活标记抗原，也表达于活化的巨噬细胞和中性粒细胞上，这表明 CD69 可能在炎症性疾病中发挥作用。为了确定 CD69 缺失对博来霉素（BLM）诱导的肺损伤的影响，我们评估了气管内 BLM 给药后的炎症反应以及随后在野生型（WT）和 CD69 缺陷型（CD69-/-）小鼠中的纤维化变化。

方法

小鼠接受 3mg/kg 体重的 BLM 单次剂量，并在气管内滴注后 7 或 14 天（dpi）处死。通过支气管肺泡灌洗液的差异细胞计数和细胞因子阵列分析来研究急性相（7dpi）的肺炎症。此外，在 14dpi 通过组织病理学和胶原测定来评估肺纤维化变化。我们还使用逆转录聚合酶链反应来测量 BLM 处理小鼠肺中转化生长因子β1（TGF-β1）的 mRNA 表达水平。

结果

与 WT 小鼠相比，CD69-/-小鼠的肺损伤较小，表现在以下指标降低：（1）体重减轻，（2）肺湿/干比，（3）BALF 中的细胞因子水平，（4）肺损伤的组织学证据，（5）肺胶原沉积，和（6）肺中 TGF-β1 mRNA 表达。

结论

本研究清楚地表明，CD69 在 BLM 诱导的肺损伤进展中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f0/3198935/75700d5d2cd5/1465-9921-12-131-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f0/3198935/9dcaab8be3a2/1465-9921-12-131-1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f0/3198935/75700d5d2cd5/1465-9921-12-131-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f0/3198935/9dcaab8be3a2/1465-9921-12-131-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f0/3198935/c70f1a9b8b76/1465-9921-12-131-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f0/3198935/428f270d8ac5/1465-9921-12-131-3.jpg
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