Arabinoxylan activates Dectin-1 and modulates particulate β-glucan-induced Dectin-1 activation

Arabinoxylan is one of the most commonly consumed dietary fiber. Immunomodulation by arabinoxylan is documented but the mechanisms by which these immune-effects are accomplished are unknown.

By applying reporter cell lines for Toll-like receptors (TLRs) and Dectin-1, we demonstrated that arabinoxylan interacts with Dectin-1 receptors and not with TLRs. Arabinoxylan activates Dectin-1 to a similar magnitude as soluble β-glucans. Soluble β-glucans are known to inhibit the particulate β-glucan-induced activation of Dectin-1. As arabinoxylan is also soluble, the inhibiting capacity of arabinoxylan on particulate β-glucan-activated Dectin-1 cell lines was studied. It was found that this inhibition was similar to that of soluble β-glucan and was caused predominantly by inhibition of the Dectin-1A transcript variant. The Dectin-1 inhibitory function of arabinoxylan was further confirmed in human dendritic cells that demonstrated reduced production of IL-10 and TNF-α. The production of the antifungal cytokines IL-4 and IL-23 were increased in dendritic cells stimulated with arabinoxylan and particulate β-glucan. In contrast to soluble β-glucan, arabinoxylan did not enhance production of IL-10, TNF-α, and IL-23.

Arabinoxylan activates Dectin-1 and supports antifungal immune responses in human dendritic cells. The mode of action of arabinoxylan is similar but not identical to that of soluble β-glucans.