Medical Inflammation Research, MediCity Research Laboratory, University of Turku, FI-20520, Turku, Finland.
Aarhus University, Department of Biomedicine, Høegh-Guldbergs Gade 10, 8000, Aarhus, Denmark.
Commun Biol. 2022 May 12;5(1):449. doi: 10.1038/s42003-022-03376-y.
Common infections and polysaccharides, from bacteria and yeasts, could trigger psoriasis and psoriatic arthritis (PsA), and possibly rheumatoid arthritis (RA). The objective of this study was to investigate the effects of β-glucan polysaccharides in the effector phase of arthritis and as regulators of psoriasis and PsA-like symptoms in mice. Collagen antibody induced arthritis was studied as a model of RA and mannan-induced psoriasis (MIP) was used as model for psoriasis and PsA, using mice with a mutation of Ncf1 on the B10.Q genetic background, making them highly disease susceptible. The mice were exposed to three common variants: 1,6-β-glucan, 1,3-β-glucan and 1,3-1,6-β-glucan. These β-glucans down-regulated disease in mice if administered simultaneously, before or after mannan. Interestingly, the protection was macrophage mannose receptor (MMR/CD206) dependent with a more pronounced protection long-term than short-term. The number of resident peritoneal macrophages decreased after in vivo challenge with β-glucan and mannan compared to mannan alone, whereas the numbers of infiltrating cells correspondingly increased, further indicating macrophages as key for β-glucan mediated regulation. At the doses tested, β-glucans could not induce arthritis, psoriasis or PsA in wild-type mice. However, β-glucans could ameliorate the PsA-like symptoms representing a new unforeseen possibility to explore for future clinical treatment.
常见的感染和多糖，来自细菌和酵母，可能引发银屑病和银屑病关节炎（PsA），并可能引发类风湿关节炎（RA）。本研究的目的是研究β-葡聚糖多糖在关节炎效应期的作用，以及作为调节银屑病和银屑病样症状的作用在小鼠中。胶原抗体诱导的关节炎被研究为 RA 的模型，甘露聚糖诱导的银屑病（MIP）被用于银屑病和银屑病关节炎的模型，使用在 B10.Q 遗传背景下 Ncf1 突变的小鼠，使它们高度易患疾病。这些β-葡聚糖有三种常见的变体：1,6-β-葡聚糖、1,3-β-葡聚糖和 1,3-1,6-β-葡聚糖。如果在甘露聚糖之前、同时或之后给药，这些β-葡聚糖可以下调疾病在小鼠中的表达。有趣的是，保护作用依赖于巨噬细胞甘露糖受体（MMR/CD206），并且长期保护比短期保护更明显。与单独使用甘露聚糖相比，β-葡聚糖和甘露聚糖体内挑战后腹膜常驻巨噬细胞数量减少，而浸润细胞数量相应增加，这进一步表明巨噬细胞是β-葡聚糖介导调节的关键。在测试的剂量下，β-葡聚糖不能诱导野生型小鼠发生关节炎、银屑病或银屑病关节炎。然而，β-葡聚糖可以改善银屑病样症状，这代表了未来临床治疗的一种新的意想不到的可能性。
