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Expression of the Immunomodulator IL-10 in Type I Pneumocytes of the Rat: Alterations of IL-10 Expression in Radiation-induced Lung Damage

Michael G. Haase, Anke Klawitter, Peter Geyer and Gustavo B. Baretton

OncoRay Center for Radiation Research in Oncology (MGH), Department of Pathology (MGH,AK,GBB), and Clinic for Radiotherapy and Radiation Oncology (PG), Dresden University of Technology, Dresden, Germany

Correspondence to: Michael Haase, OncoRay Center for Radiation Research in Oncology, Medical Faculty, Dresden University of Technology, Fetscherstrasse 74, 01307 Dresden, Germany. E-mail: Michael.Haase{at}OncoRay.de

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 and also in a pro-fibrotic way by activating TH2 cytokines. (J Histochem Cytochem 55:1167–1172, 2007)

Key Words: interleukin-10 • type I pneumocytes • fibrosing alveolitis • radiation damage

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