Schizophyllum commune β-glucan: Effect on interleukin-10 expression induced by lipopolysaccharide from periodontopathic bacteria

[Display omitted] •SPG elevates LPS-induced IL-10 expression via dectin-1 receptor.•SPG up-regulates IL-10 expression by enhancing NF-kB and MSK1 activities.•Syk is required for MSK1 and CREB phosphorylation by SPG.•SPG regulates inflammation caused by periodontitis. β-glucans are potent immunomodul...

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Veröffentlicht in:Carbohydrate polymers 2021-02, Vol.253, p.117285-117285, Article 117285
Hauptverfasser: Thongsiri, Chuencheewit, Nagai-Yoshioka, Yoshie, Yamasaki, Ryota, Adachi, Yoshiyuki, Usui, Michihiko, Nakashima, Keisuke, Nishihara, Tatsuji, Ariyoshi, Wataru
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Sprache:eng
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Zusammenfassung:[Display omitted] •SPG elevates LPS-induced IL-10 expression via dectin-1 receptor.•SPG up-regulates IL-10 expression by enhancing NF-kB and MSK1 activities.•Syk is required for MSK1 and CREB phosphorylation by SPG.•SPG regulates inflammation caused by periodontitis. β-glucans are potent immunomodulators, with effects on innate and adaptive immune responses via dectin-1 as the main receptor. In this study, we investigated the biological effect of β-glucan from Schizophyllum commune, called Schizophyllan (SPG) on Interleukin-10 (IL-10) expression induced by a lipopolysaccharide (LPS) from Aggregatibacter actinomycetemcomitans in murine macrophages (J774.1). SPG and dectin-1 interaction up-regulates LPS-induced IL-10 expression. The regulative effect of SPG on IL-10 expression is dependent on prolongation of nuclear translocation activity of nuclear factor-kappa B (NF-κBα) pathway induced by LPS. We also found that LPS-induced phosphorylation of mitogen- and stress-activated protein kinase 1 (MSK1) and cAMP-responsive-element-binding protein (CREB), followed by up-regulation of IL-10, was stimulated by SPG priming via activation of the spleen tyrosine kinase (Syk). Our data indicate that SPG augments the anti-inflammatory response in murine macrophages which can be useful to create an intervention for periodontal disease treatment.
ISSN:0144-8617
1879-1344
DOI:10.1016/j.carbpol.2020.117285