Neha M Sahasrabudhe1, Henk A Schols2, Marijke M Faas1,3, Paul de Vos1. 1. Division of Medical Biology, Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. 2. Laboratory of Food Chemistry, Wageningen University, Wageningen, Gelderland, The Netherlands. 3. Department of Obstetrics and Gynaecology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Abstract
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.
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.
Authors: M B Gea Kiewiet; Renske Dekkers; Marjan Gros; R J Joost van Neerven; Andre Groeneveld; Paul de Vos; Marijke M Faas Journal: PLoS One Date: 2017-06-08 Impact factor: 3.240
Authors: Neha M Sahasrabudhe; Martin Beukema; Lingmin Tian; Berit Troost; Jan Scholte; Erik Bruininx; Geert Bruggeman; Marco van den Berg; Anton Scheurink; Henk A Schols; Marijke M Faas; Paul de Vos Journal: Front Immunol Date: 2018-03-01 Impact factor: 7.561
Authors: Mensiena B G Kiewiet; Renske Dekkers; Martine P van Gool; Laurien H Ulfman; Andre Groeneveld; Marijke M Faas; Pau de Vos Journal: Mol Nutr Food Res Date: 2018-11-02 Impact factor: 5.914