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