Bacterial β-(1,3)-glucan prevents DSS-induced IBD by restoring the reduced population of regulatory T cells

Lee, Kwang-Ho; Park, Min; Ji, Kon-Young; Lee, Hwa-Youn; Jang, Ji-Hun; Yoon, Il-Joo; Oh, Seung-Su; Kim, Su-Man; Jeong, Yun‐Hwa; Yun, Chul‐Ho; Kim, Mi-Kyoung; Lee, In-Young; Choi, Hyungsub; Ko, Kisung; Kang, Hyung‐Sik

doi:10.1016/j.imbio.2014.07.003

Cited by 41 publications

(32 citation statements)

References 54 publications

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“…Inflammatory bowel diseases (IBD), characterized by rectal bleeding, diarrhea, intestinal motility disorder, and colonic shortening, are linked with colonic chronic inflammation [1, 2]. Recently, Intestinal macrophages and dendritic cells have been indicated to involve in the initiation of inflammation in IBD through inappropriate responses to enteric microbial stimuli, inefficient clearance of microbes from host tissues, and impaired transition from appropriate proinflammatory responses to anti-inflammatory responses [3–5].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice

Zhao

Liu²,

Tan

et al. 2018

Inflamm. Res.

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BackgroundAdiponectin, a protein hormone produced by adipose tissues, exhibits anti-inflammatory functions in various models. This study was investigated the effects of adiponectin on dextran sodium sulfate (DSS)-colonic injury, inflammation, apoptosis, and intestinal barrier dysfunction in Caco-2 cell and mice.Materials and methodsThe results showed that DSS caused inflammatory response and intestinal barrier dysfunction in vitro and in vivo. Adiponectin injection alleviated colonic injury and rectal bleeding in mice. Meanwhile, adiponectin downregulated colonic IL-1β and TNF-α expressions and regulated apoptosis relative genes to attenuate DSS-induced colonic inflammation and apoptosis. Adiponectin markedly reduced serum lipopolysaccharide concentration, a biomarker for intestinal integrity, and enhanced colonic expression of tight junctions (ZO-1 and occludin). The in vitro data further demonstrated that adiponectin alleviated DSS-induced proinflammatory cytokines production and the increased permeability in Caco-2 cells.ConclusionAdiponectin plays a beneficial role in DSS-induced inflammation via alleviating apoptosis and improving intestinal barrier integrity.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice

Zhao

Liu²,

Tan

et al. 2018

Inflamm. Res.

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“…Fig. 1, altered body weight, colon length and weight, rectal bleeding and histological scores indicated a colitis model, which is consistent with previous studies (18,19). Compared with the IBD group, urantide injection markedly reduced rectal bleeding and histological scores after DSS treatment, suggesting a protective role in the colitis model.…”

Section: Methodssupporting

confidence: 90%

UII/GPR14 is involved in NF-κB-mediated colonic inflammation in vivo and in vitro

et al. 2016

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The present study was conducted to investigate the molecular mechanism of urotensin II (UII) and its receptor, G protein‑coupled receptor 14 (GPR14), in colonic inflammation. Urantide, a special antagonist of GPR14, and GPR14-siRNA were used to inhibit GPR14 signaling in dextran sulfate sodium (DSS)‑induced inflammation in mice and Caco-2 cells. The results showed that urantide alleviated rectal bleeding, histological injury and production of interleukin (IL)-17 and tumor necrosis factor‑α (TNF‑α) caused by DSS in mice. GPR14-siRNA transfection subsequent with GPR14 inhibition reduced DSS-induced interferon-γ (IFN)-γ production in Caco-2 cells. Meanwhile, both in vivo and in vitro data demonstrated that inhibition of UII/GPR14 alleviated nuclear factor-κB (NF-κB) activation caused by DSS. In conclusion, UII/GPR14 signaling was involved in the DSS-induced colonic inflammation and its inhibition may serve as a potential therapeutic target, which may be associated with the NF-κB signaling pathway.

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“…The immunomodulatory, anti‐inflammatory and anti‐carcinogenic effects of glucans, which are abundantly found in edible mushrooms, have been reported in numerous studies. These polysaccharides show high efficacy and low toxicity than other therapeutic agents in clinical use . Lentinan is an anti‐tumour polysaccharide from Lentinula edodes , which is highly effective against DSS‐induced acute colitis .…”

Section: Discussionmentioning

confidence: 99%

“…These polysaccharides show high efficacy and low toxicity than other therapeutic agents in clinical use. 43,44 Lentinan is an anti-tumour polysaccharide from Lentinula edodes, which is highly effective against DSS-induced acute colitis. 20 In the present study, lentinan suppressed body weight loss and colon length shortening and improved histological scores in DSS-induced acute colitis, chronic colitis and TNBS-induced model mice.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic effects of lentinan on inflammatory bowel disease and colitis‐associated cancer

Liu

Zhao

et al. 2018

J Cellular Molecular Medi

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In this study, we investigated the therapeutic potential of lentinan in mouse models of inflammatory bowel disease (IBD) and colitis‐associated cancer (CAC). Lentinan decreased the disease activity index and macroscopic and microscopic colon tissue damage in dextran sulphate sodium (DSS)‐induced or TNBS‐induced models of colitis. High‐dose lentinan was more effective than salicylazosulfapyridine in the mouse models of colitis. Lentinan decreased the number of tumours, inflammatory cell infiltration, atypical hyperplasia and nuclear atypia in azoxymethane/DSS‐induced CAC model. It also decreased the expression of pro‐inflammatory cytokines, such as IL‐13 and CD30L, in IBD and CAC model mice possibly by inhibiting Toll‐like receptor 4 (TLR4)/NF‐κB signalling and the expression of colon cancer markers, such as carcinoembryonic antigen, cytokeratin 8, CK18 and p53, in CAC model mice. In addition, lentinan restored the intestinal bacterial microbiotal community structure in IBD model mice. Thus, it shows therapeutic potential in IBD and CAC model mice possibly by inhibiting TLR4/NF‐κB signalling‐mediated inflammatory responses and disruption of the intestinal microbiotal structure.

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Bacterial β-(1,3)-glucan prevents DSS-induced IBD by restoring the reduced population of regulatory T cells

Cited by 41 publications

References 54 publications

RETRACTED ARTICLE: Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice

RETRACTED ARTICLE: Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice

UII/GPR14 is involved in NF-κB-mediated colonic inflammation in vivo and in vitro

Therapeutic effects of lentinan on inflammatory bowel disease and colitis‐associated cancer

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