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Arabinoxylan activates Dectin‐1 and modulates particulate β‐glucan‐induced Dectin‐1 activation
Author(s) -
Sahasrabudhe Neha M.,
Schols Henk A.,
Faas Marijke M.,
Vos Paul
Publication year - 2016
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201500582
Subject(s) - arabinoxylan , glucan , immune system , chemistry , receptor , biochemistry , microbiology and biotechnology , biology , polysaccharide , immunology
Scope 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. Methods and results 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. Conclusion 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.