Expression of the immunomodulator IL-10 in type I pneumocytes of the rat: Alterations of IL-10 expression in radiation-induced lung damage

被引:12
作者
Haase, Michael G.
Klawitter, Anke
Geyer, Peter
Baretton, Gustavo B.
机构
[1] Tech Univ Dresden, Fac Med, OncoRay Ctr Radiat Res Oncol, D-01307 Dresden, Germany
[2] Tech Univ Dresden, Dept Pathol, D-8027 Dresden, Germany
[3] Tech Univ Dresden, Clin Radiotherapy & Radiat Oncol, D-8027 Dresden, Germany
关键词
interleukin-10; type I pneumocytes; fibrosing alveolitis; radiation damage;
D O I
10.1369/jhc.7A7173.2007
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Fibrosing alveolitis is a disease with inflammatory, proliferative, and fibrotic components. In different models, it has been shown that the cytokine interleukin-10 (IL-10) plays a conflicting role in inflammation-associated fibrotic processes, inasmuch as it is an anti-inflammatory cytokine but also a TH2 cytokine with inherent pro-fibrotic effects. IL-10 is produced primarily by inflammatory cells. In this report, we show in a rat model of radiation-induced fibrosing alveolitis that IL-10 is also produced by type I alveolar epithelial cells in both normal and fibrotic lungs. The total amount of IL-10 in the lung is increased after irradiation, but type I pneumoyctes contain less IL-10. The R3/1 permanent type I pneumocyte cell line also contains IL-10, which is reduced after irradiation. Whereas in the normal lung, the entire alveolar surface is covered by IL-10-producing pneumocytes, this continuity is interrupted in fibrotic lungs, because type I pneumocytes lack full differentiation and thus full spreading over the alveolar surface. The exposure of the IL-10-negative epithelial basal membrane may allow for an easier attachment of inflammatory cells such as alveolar macrophages. These cells have the potential to act in a pro-inflammatory way by tumor necrosis factor at and also in a pro-fibrotic way by activating TH2 cytokines.
引用
收藏
页码:1167 / 1172
页数:6
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