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Investigations on the role of inflammatory cytokines in EMT and cell migration in alveolar epithelial cells

Epithelial‐mesenchymal transition (EMT), a process through which epithelial cells lose their polarity and become motile mesenchymal cells, is a contributory factor in fibrosis. Growth factors and inflammatory cytokines are purported to orchestrate this process. Here the ability of TGF‐β1 and inflammatory cytokines to induce EMT and their effect on cell migration was assessed. Alveolar epithelial cells (A549) were stimulated with TGF‐β1 and/or cytomix [CM; IL‐1β + TNF‐α + IFN‐γ]. Alterations in cell morphology and changes in expression of EMT markers were measured. The influence of TGF‐β1, IL‐1β, TNF‐α and IFN‐γ (alone and in combinations) on cell migration was determined by wound closing assay. Control cells exhibited an epithelial morphology with expression of E‐cadherin and an absence of α‐SMA. Treatment with TGF‐β1 induced EMT with cells adopting a spindle‐shaped phenotype. This was coupled with a down regulation of E‐cadherin expression and an up‐regulation of α‐SMA. CM, either alone or in combination with TGF‐β1, was found to induce EMT to a greater extent than TGF‐β1. CM, IL‐1β + TNF‐α and IL‐1β alone were all found to significantly (P<0.001) enhance cell migration. TGF‐β1 had little effect, either alone or when added to different combinations of cytokines. Our results suggest that inflammatory cytokines together with TGF‐β1 may play an important role in the development of fibrosis via the mechanism of EMT.