Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9110882 | Cytokine | 2005 | 9 Pages |
Abstract
Recent work carried out in our laboratory showed the existence of a cytokine storm in SARS patients, dominated by Th1-type mediators. We thus hypothesized that IFN-γ may play a major role in the pathology by triggering immune-mediated alveolar damage. As we assessed or re-assessed some effects of IFN-γ on a number of human lung epithelial and fibroblast cell lines, chosen for their wide use in the literature, we found that alveolar epithelial cells were more sensitive to IFN-γ, in terms of proliferation inhibition and enhancement of Fas-mediated apoptosis. While similar effects were obtained on fibroblasts, concentrations of IFN-γ 4-8-fold greater were required. In addition, both epithelial and fibroblastic cell lines were able to secrete large quantities of T cell-targeting chemokines, similar to the ones detected in SARS patients. Based on the clinical data collected previously, the available literature and our in vitro experimentation, we propose that IFN-γ may be responsible for acute lung injury in the late phase of the SARS pathology.
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Authors
Michel Theron, Kao-Jean Huang, Yu-Wen Chen, Ching-Chuan Liu, Huan-Yao Lei,