Silica-induced chemokine expression in alveolar type II cells is mediated by TNF-α.
نویسندگان
چکیده
Recent evidence has suggested that epithelial cells may contribute to the inflammatory response in the lung after exposure to crystalline silica through the production of and response to specific growth factors, chemokines, and cytokines. However, the exact cellular and molecular responses of epithelial cells to silica exposure remains unclear. Using a murine alveolar type II cell line [murine lung epithelial (MLE)-15 cell line], we measured the early changes in various cytokine and chemokine mRNA species after exposure of the cells to 4-35 μg/cm2 of silica (cristobalite), interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and lipopolysaccharide (LPS) alone or in combination. Total mRNA was isolated and assayed with an RNase protection assay after 6 and 24 h of exposure. Cristobalite exposure alone led to an increase in monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-2, and regulated on activation normal T cells expressed and secreted (RANTES) mRNAs. Treatment with IFN-γ alone increased MCP-1 mRNA levels. Treatment with TNF-α or LPS alone led to an increase in MCP-1 and MIP-2 mRNA. The combination of cristobalite plus TNF-α led to an additive increase in MCP-1 and MIP-2, whereas cristobalite plus IFN-γ or LPS had a synergistic effect. We also found with a TNF-α-neutralizing antibody that TNF-α plays a major role in mediating the type II cell chemokine response to cristobalite exposure. The results indicate that the cristobalite-induced chemokine response in the lung epithelium is mediated in part by TNF-α and can be enhanced by macrophage- and lymphocyte-derived inflammatory mediators in an additive and synergistic fashion.
منابع مشابه
Silica-induced chemokine expression in alveolar type II cells is mediated by TNF-α-induced oxidant stress.
We have shown previously that epithelial cells may contribute to the inflammatory response in the lung after exposure to crystalline silica through the production of and response to specific chemokines and cytokines. However, the exact cellular and molecular responses of epithelial cells to silica exposure remain unclear. We hypothesize that non-oxidant-mediated silica-cell interactions lead to...
متن کاملSilica-induced chemokine expression in alveolar type II cells is mediated by TNF-a-induced oxidant stress
Barrett, Edward G., Carl Johnston, Günter Oberdörster, and Jacob N. Finkelstein. Silica-induced chemokine expression in alveolar type II cells is mediated by TNF-ainduced oxidant stress. Am. J. Physiol. 276 (Lung Cell. Mol. Physiol. 20): L979–L988, 1999.—We have shown previously that epithelial cells may contribute to the inflammatory response in the lung after exposure to crystalline silica th...
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ورودعنوان ژورنال:
- American journal of physiology. Lung cellular and molecular physiology
دوره 275 6 شماره
صفحات -
تاریخ انتشار 1998