Description:
Interleukin 17F (IL17F) has been found to be involved in various inflammatory pathologiesand has recently become a target for therapeutic purposes. In contrast to IL17F secreted by immunecells, the focus of this study is to describe the triggers of IL17F release in non-immune cells with aparticular focus on IL17F-induced fibrosis. IL17F induction was examined in human lung epithelial(BEAS-2B) and myeloid cell lines as well as in peripheral blood mononuclear cells after in vitroexposure to aqueous cigarette smoke extract (CSE), inorganic mercury, cadmium or the apoptosisinducer brefeldin A. Fibrosis was examined in vitro, evaluating the transition of human primarydermal fibroblasts to myofibroblasts. We observed that all stressors were able to induce IL17F geneexpression regardless of cell type. Interestingly, its induction was associated with cytotoxic/apoptoticsigns. Inhibiting oxidative stress by N-acetylcysteine abrogated CSE-induced cytotoxic and IL17F-inducing effects. The induction of IL17F was accompanied by IL17F protein expression. The transitionof fibroblasts into myofibroblasts was not influenced by either recombinant IL17F or supernatants ofCSE-exposed BEAS-2B. In addition to IL17F secretion by specialized or activated immune cells, weunderscored the cell type-independent induction of IL17F by mechanisms of inhibitable oxidativestress-induced cytotoxicity. However, IL17F was not involved in dermal fibrosis under the conditions used in this study.