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 of T. 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 mu g/ml beta-glucan stimulation for 24 h significantly increased CXCL8, CXCL11, and IL-1 beta secretions in KC. Furthermore, beta-glucan exposure induced the expressions of JAK2 mRNA, STAT3 mRNA, and p-STAT3 protein. Silencing JAK2 expression inhibited p-STAT3 protein expression and beta-glucan-induced IL-1 beta secretion. And overexpression of JAK2 further promoted beta-glucan-mediated p-STAT3 protein and IL-1 beta productions. These results suggested that beta-glucan-induced CXCL8, CXCL11, and IL-1 beta secretions in rabbit KC might be involved in the inflammatory response of T. mentagrophytes infected rabbit dorsal skin. However, only IL-1 beta 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.