Anti-allergic Effect of Soluble Beta-glucan on Japanese Cedar Pollinosis and Mechanism Underlying Its Allergy-ameliorating Action
Mutsumi Tanaka, Tetsu Sawamoto, Keiko Mizuyama, Fusako Mitsunaga, Shin NakamuraiD
Abstract
Japanese cedar (sugi) pollinosis is triggered by sensitization to sugi pollen, which contains sugi antigens, sugi basic proteins (SBP: Cryj1 and Cryj2), and adjuvant polysaccharides, insoluble {beta}-glucan particles (IBG: a dectin-1 agonist). The presence of IBG in sugi pollen enhances the production of SBP-specific IgE, which participates in inflammatory response via activation of mast cells to lead to their degranulation, resulting in sneezing. Another {beta}-glucan derived from black yeast, soluble {beta}-glucan (SBG: a dectin-1 antagonist), is known to have an anti-allergic function. Herein, we demonstrated that oral administration of SBG suppressed both SBP-specific IgE production and SBP-induced sneeze in sugi pollinosis mice model. DNA microarray analyses revealed previously unknown mechanisms underlying SBG-mediated anti-allergy action. SBG ameliorated the dysregulated expression of 16 immune-inflammatory genes that were unusually either up- or down-regulated in sugi pollinosis mice. Based on the DNA microarray informatics, it was suggested that SBG mitigated the IBG-mediated hyper-response of IgE production and inflammatory reaction in immune-inflammatory cells, B and T cells, antigen-presenting cells, and granulocytes (neutrophils and eosinophils) within iliac lymph nodes. The SBG-mediated inhibition of SBP-induced sneezing in pollinosis mice results from a decline in SBP-specific IgE level. The oral administration of SBG influenced gut microbiota, notably enhancing beneficial bacteria such as bifidobacteria. Consequently, it is plausible that short-chain fatty acids, produced by these beneficial bacteria, inhibited mast cell degranulation, leading to a reduction in sneezing. Collectively, SBG demonstrated anti-allergic effects against sugi pollinosis by inhibiting the immune response, specifically SBP-induced IgE production, as well as reducing the inflammatory reaction characterized by SBP-induced sneezing.
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