Heat‐shock pretreatment reduces expression and release of TSLP from keratinocytes under Th2 environment

Abstract Background Atopic dermatitis is a chronic, relapsing inflammatory disease of the skin. Current therapy is not curative, and recalcitrant disease is a big stress and challenge for parents and physicians. This study explored the potential role of heat‐shock protein 70 ( HSP ‐70) and its anti‐inflammatory effects on keratinocyte under TH 2 environment. Methods Human keratinocyte cell line (HaCa T) was stimulated with IL ‐4, IL ‐13, and TNF ‐α to synthesize and secrete thymic stromal lymphopoietin ( TSLP ), an important cytokine of immunopathogenesis in atopic dermatitis. Heat shock was performed by immersing the cell‐contained flash into a water bath of 45°C for 20 min. Cell viability, TSLP expression, and secretion of HaCa T cells were measured and compared. Possible regulatory mechanisms influencing the expression of TSLP , such as the STAT 6 and NF ‐κB signal pathways, were investigated. Results Heat‐shock treatment induced intracellular HSP ‐70 expression in HaCa T cells without affecting cell viability. The induced expression and secretion of TSLP in HaCa T cells were suppressed by heat shock. The NF ‐κB signal pathway was inhibited by heat shock, leading to decreased TSLP expression and secretion. Conclusion Heat stress‐induced HSP s can significantly reduce the production and secretion of TSLP from HaCaT cells under Th2 environment. Thus, the evidence highlights the potential role of HSP ‐70 for atopic dermatitis in the future.