Novel probiotic yeast from Miso promotes regulatory dendritic cell IL-10 production and attenuates DSS-induced colitis in mice

Okada, Yoshikiyo; Tsuzuki, Yoshikazu; Sugihara, Nao; Nishii, Shin; Shibuya, Naoki; Mizoguchi, Akinori; Itoh, Suguru; Tanemoto, Rina; Inaba, Kenichi; Hanawa, Yoshinori; Horiuchi, Kazuki; Wada, Akinori; Higashiyama, Masaaki; Watanabe, Chikako; Kurihara, Chie; Komoto, Shunsuke; Tomita, Kengo; Miura, Soichiro; Hokari, Ryota

doi:10.1007/s00535-021-01804-0

Cited by 16 publications

(24 citation statements)

References 39 publications

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“…LP-DCs continuously take up antigens from the intestine and migrate to the draining mesenteric lymph nodes (MLNs), where they present antigens to T cells to further drive different T-cell fates ( Coombes and Powrie, 2008 ). DC with low expression of MHC-II, CD86 and CD80 and high expression of IL-10 can improve colonic inflammation and reduce local lesion injury, which is related to the decrease of CD4 + T cell number in the colon and the differentiation of naive T cells into Foxp3 Treg cells ( Jin et al, 2019 ; Okada et al, 2021 ; Rao et al, 2022 ). Our results showed that in the DSS-induced inflammatory microenvironment, the proportion of infiltrating DCs and the reduction of MHC-II + expressing DCs in the colon of WGP-treated mice were significantly increased compared with CON mice.…”

Section: Discussionmentioning

confidence: 99%

Whole β-glucan particle attenuates AOM/DSS-induced colorectal tumorigenesis in mice via inhibition of intestinal inflammation

Xie

Shao²,

Duan³

et al. 2023

Front. Pharmacol.

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Yeast β-glucan is a polysaccharide purified from the Saccharomyces cerevisiae cell wall, and its multiple biological activities are essential for immune regulation. However, the effect of β-glucan on the intestinal immune response during colitis-associated colorectal cancer (CAC) is unclear. Here, we explore the possible role of β-glucan in the development of CAC. Wild type (WT) mice with CAC induced by azoxmethane (AOM) and dextran sodium sulfate (DSS) had fewer tumors than untreated mice after oral β-glucan because of increased antitumor dendritic cells (DCs) in the tumor microenvironment, resulting in more CD8+ T cells and the production of related cytokines. β-glucan also increased resistance to DSS-induced chronic colitis by reshaping the inflammatory microenvironment. These data suggest that β-glucan improves experimental intestinal inflammation and delays the development of CAC. Therefore, β-glucan is feasible for treating chronic colitis and CAC in clinical practice.

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Section: Discussionmentioning

confidence: 99%

Whole β-glucan particle attenuates AOM/DSS-induced colorectal tumorigenesis in mice via inhibition of intestinal inflammation

Xie

Shao²,

Duan³

et al. 2023

Front. Pharmacol.

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“…We observed that Rs significantly inhibited the signals of the IL-10 expression pathway in DCs. IL-10 is the chief player of the tolerogenic properties in DCs 24 . The insufficient expression of IL-10 caused by Rs generates a substantial impact on the SIT-induced tolerogenic feature in DCs.…”

Section: Discussionmentioning

confidence: 99%

Targeting psychological stress-steroid-MARCH1 signaling pathway promotes the efficacy of specific allergen immunotherapy

Liu²,

Xiao³

et al. 2022

Theranostics

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Background:The therapeutic efficacy of allergen specific immunotherapy (SIT) is recognized, but needs improved. Psychological stress influences the immune system's function. The objective of this study is to elucidate the effects of psychological stress on compromising the effectiveness of SIT. Methods: A murine model with the airway allergic disorder (AAD) was established. Mice were treated with SIT with or without restraint stress (Rs). Results: Rs was found to significantly hamper the efficacy of SIT in mice with AAD. Induction of IL-10 + dendritic cells and type 1 regulatory T cells were reduced by Rs in the airway tissues. Rs-induced cortisol release subverted immune tolerance generation. Expression of MARCH1 was elevated in dendritic cells of the allergic lesion sites. The Rs-induced MARCH1 mediated the immune impairment in AAD mice. Genetic ablation of MARCH1 in dendritic cells efficiently blocked the Rs-compromised the therapeutic efficacy of SIT. Conclusion: Rs can increase the expression of MARCH1 in DCs of the allergic lesion sites. MARCH1 interferes with the immune regulatory properties in DCs, and impairs the immune regulatory capacity. Blocking MARCH1 can counteract the Rs-affected SIT efficacy.

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“…Defects of IL-10, IL-10-receptor-A and IL-10-receptor-B genes represent a major cause of early-onset IBD [ 35 , 36 ]. Furthermore, mice with lacking IL-10 and IL-10R are more likely to develop spontaneous colitis [ 21 , 33 , 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

MiRNA-374b-5p and miRNA-106a-5p are related to inflammatory bowel disease via regulating IL-10 and STAT3 signaling pathways

Liu

et al. 2022

BMC Gastroenterol

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Background Inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis, is one of the most frequent gastrointestinal disorders worldwide. Although the actual etiology of IBD remains unclear, growing evidence suggests that CD4+ T cells-associated cytokines, including interferon (IFN)-γ, interleukin (IL)-10 and IL-17A, are crucial for the occurrence of IBD. It has been reported that there is a positive association between miRNAs and IBD development. In this study, we investigated the roles of hsa-miRNA-374b-5p(miRNA-374b-5p) and hsa-miRNA-106a-5p(miRNA-106a-5p) in regulating IBD development. Methods Serum was obtained from vein blood of IBD patients and healthy controls, qRT-PCR was performed to study the expression of miRNA-374b-5p and miRNA-106a-5p. Furthermore, we investigate the effects of overexpression or inhibition of miRNA-374b-5p on naïve CD4 + T cell subsets differentiation from vein blood of healthy controls by RT-qPCR, flow cytometry and western blot. And more the prediction and confirmation of the targeting genes of miRNA-374b-5p and miRNA-106a-5p were performed by bioinformatics softwares and dual-luciferase reporter assay. Results The results showed that miRNA-106a-5p and miRNA-374b-5p were significantly overexpressed in IBD patients. MiRNA-374b-5p could enhance Th1/Th17 cell differentiation and was related to IBD pathogenesis. MiRNA-374b-5p overexpression induced the mRNA expression of IL-17A and IFN-γ, and suppressed that of IL-10 in T cells. MiRNA-374b-5p inhibition decreased the mRNA expression of IL-17A and IFN-γ, while upregulated that of IL-10 in T cells. These qPCR data were further verified at protein level by western blotting and flow cytometry. In addition, dual-luciferase reporter (DLR) assay indicated that miRNA-374b-5p was directly targeted by IL-10, a key anti-inflammatory cytokine for preventing the occurrence of IBD. Meanwhile, STAT3 was identified as a target gene of miRNA-106a-5p by DLR assays. Further analysis revealed that miRNA-374b-5p regulated JAK1 and STAT3 pathways in CD4+ T cells via IL-10/STAT3 axis. MiRNA-374b-5p overexpression remarkably decreased the mRNA expression and phosphorylated (ser-727) protein levels of STAT3, while miRNA-374b-5p inhibition had the opposite effects. Conclusion MiRNA-374b-5p and miRNA-106a-5p may contribute to IBD development by regulating IL-10/STAT3 signal transduction.

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Novel probiotic yeast from Miso promotes regulatory dendritic cell IL-10 production and attenuates DSS-induced colitis in mice

Cited by 16 publications

References 39 publications

Whole β-glucan particle attenuates AOM/DSS-induced colorectal tumorigenesis in mice via inhibition of intestinal inflammation

Whole β-glucan particle attenuates AOM/DSS-induced colorectal tumorigenesis in mice via inhibition of intestinal inflammation

Targeting psychological stress-steroid-MARCH1 signaling pathway promotes the efficacy of specific allergen immunotherapy

MiRNA-374b-5p and miRNA-106a-5p are related to inflammatory bowel disease via regulating IL-10 and STAT3 signaling pathways

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