β-glucan augments IL-1β production by activating the JAK2/STAT3 pathway in cultured rabbit keratinocytes

Trichophyton mentagrophytes(T. mentagrophytes) is the main cause of rabbit dermatophytosis. As the main pathogen-associated molecular pattern ofT. mentagrophytes, the role of beta-glucan in the pathogenesis of rabbit dermatophytosis remains elusive. Keratinocytes (KC) are the main cellular component and the first defensive line against fungal pathogens in the skin. Therefore, the present study investigated the effects of beta-glucan on rabbit KC from dorsal skin. beta-glucan was found to inhibit KC proliferation by 10% at 20 ug/ml and this concentration was thus considered as optimal. Next, 20 ug/ml beta-glucan stimulation for 24 h significantly increased CXCL8, CXCL11, and IL-1beta secretions in KC. Furthermore, beta-glucan exposure induced the expressions ofJAK2mRNA,STAT3mRNA, and p-STAT3 protein. SilencingJAK2expression inhibited p-STAT3 protein expression and beta-glucan-induced IL-1beta secretion. And overexpression ofJAK2further promoted beta-glucan-mediated p-STAT3 protein and IL-1beta productions. These results suggested that beta-glucan-induced CXCL8, CXCL11, and IL-1beta secretions in rabbit KC might be involved in the inflammatory response ofT. mentagrophytesinfected rabbit dorsal skin. However, only IL-1beta secretion was promoted by the JAK2/STAT3 signaling pathway. In conclusion, this study is a necessary step toward elucidating the mechanisms that underlie skin immune system injury stimulated by beta-glucan.