Variants of beta-glucan polysaccharides downregulate autoimmune inflammation

Abstract

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 beta-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-beta-glucan, 1,3-beta-glucan and 1,3-1,6-beta-glucan. These beta-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 beta-glucan and mannan compared to mannan alone, whereas the numbers of infiltrating cells correspondingly increased, further indicating macrophages as key for beta-glucan mediated regulation. At the doses tested, beta-glucans could not induce arthritis, psoriasis or PsA in wild-type mice. However, beta-glucans could ameliorate the PsA-like symptoms representing a new unforeseen possibility to explore for future clinical treatment.beta-glucan exerted anti-inflammatory activities in a murine model of psoriasis and psoriatic arthritis is, at least in part, mediated via the activation of CD206 on macrophages