Saccharomyces cerevisiae β-glucan-induced SBD-1 expression in ovine ruminal epithelial cells is mediated through the TLR-2-MyD88-NF-κB/MAPK pathway

Ovine ruminal epithelial cells (ORECs) not only have a physical barrier function but also can secrete host defence peptides (HDPs), such as sheep -defensin-1 (SBD-1). As a feed additive, Saccharomyces cerevisiae can enhance the host's innate immunity. -glucan, a cell wall component of Saccharomyces cerevisiae, can stimulate innate immune responses and trigger the up-regulation of SBD-1 in ORECs. The signaling mechanisms involved in -glucan-induced SBD-1 expression are not completely understood. The aim of this study was to identify the receptors and intracellular pathways involved in the up-regulation of SBD-1 induced by -glucan. ORECs were cultured, and the regulatory mechanisms of -glucan-induced up-regulation of SBD-1 were detected using quantitative real-time PCR (qPCR), enzyme-linked immunosorbent assay (ELISA), and western blotting. TLR-2 and MyD88 knockdown or inhibition attenuated -glucan-induced SBD-1 expression. We also showed that inhibition of MAPK and NF-B pathways significantly reduced -glucan-induced SBD-1 expression. These results demonstrate that -glucan-induced SBD-1 expression is TLR-2-MyD88-dependent and may be regulated by both MAPK and NF-B pathways. Since NF-B inhibition had a greater effect on the down-regulation of -glucan-induced SBD-1 expression, the NF-B pathway may be the dominant signaling pathway involved in the regulation of defensin expression. Our studies demonstrate that -glucan-induced SBD-1 expression is mediated through the TLR-2-MyD88-NF-B/MAPK pathway. Our results would contribute to the understanding of immunological modulations in the gastrointestinal tract triggered by probiotic yeast cell wall components.