TSLP reduced neuroinflammation by blocking the activation of microglia in the JAK2/STAT5 pathway

Abstract

Abstract The thymic stromal lymphopoietin (TSLP) in the central nervous system is highly expressed in response to inflammation but the function of TSLP is still unclear. Using the LPS-stimulated microglia model, we measured oxidative stress, microglial activation markers, and inflammatory indexes to examine the direct impact of TSLP on LPS-stimulated microglia activation as well as the underlying mechanism. The results demonstrated that TSLP treatment decreased LPS-induced oxidative stress, inflammation, and the expression of M1-type markers in microglia by increasing TSLP receptor expression. The results also showed that TSLP treatment could control the differentiation of microglia toward M2 type by preventing the activation of microglia in the JAK2/STAT5 pathway with the presence of LPS, even though TSLP may directly promote the expression of pro-inflammatory cytokines without the presence of LPS. These findings support the hypothesis that TSLP reduces neuroinflammation and blocks the JAK2/STAT5 pathway induced by LPS, revealing the regulatory role of TSLP in the central nervous system and presenting a novel strategy for the control of the inflammatory response in the central nervous system.