β-Glucan is known to have anti-inflammatory properties, and several studies have demonstrated the beneficial effects of dietary β-glucan on inflammatory bowel disease (IBD). However, it is unknown how β-glucan mediates its protective effects on IBD. Therefore, we used a well-established mouse model for IBD, interleukin (IL)-10–/– mice, to explore the protective effects of β-glucan on IBD-like symptoms caused by IL-10 deficiency. The mice were divided into two groups: IL-10–/– and IL-10–/– + β-glucan treatment groups. IL-10–/– mice treated with dietary β-glucan exhibited less inflammation within the colon. The levels of immunoglobulins A and E were lower in the serum, spleen, mesenteric lymph nodes, and Peyer's patches in the IL-10–/– mice compared with the IL-10–/– + β-glucan mice. Also, the expression of pro-inflammatory cytokines was lower in the IL-10–/– + β-glucan mice compared with the IL-10–/– mice. Histological analysis also revealed that administration of dietary β-glucan in IL-10–/– mice reduced colonic tissue damage. Finally, the expression of the pro-inflammatory cytokine tissue necrosis factor-α was significantly lower with dietary β-glucan treatment in IL-10–/– mice. In conclusion, dietary β-glucan reduces the inflammation associated with IBD caused by IL-10 deficiency.
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