秦环龙+马延磊+沈通一:植物乳杆菌抗炎蛋白MIMP或能改善肠炎
创作:大力 审核:mildbreeze 2018年10月19日
  • 微整合膜蛋白(MIMP)是植物乳杆菌表层蛋白的最小结构域;
  • 在DSS诱导小鼠结肠炎模型中,MIMP显著增加结肠长度,缓解炎症,调节促炎(IFN-γ, IL-17 和IL-23)及抗炎(IL-4 和 IL-10)炎症细胞因子的表达水平,改善菌群失调,增加紧密连接,保护肠道屏障;
  • 体外实验中,MIMP通过TLR4通路和组蛋白乙酰化,来调节炎症细胞因子表达,进而抑制LPS诱导的炎症反应,且这种作用具有时间和剂量依赖性;
  • MIMP或可用于IBD临床治疗。
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mildbreeze
由同济大学附属上海第十人民医院秦环龙、马延磊和沈通一团队共同主导的研究,发现来自植物乳杆菌的微整合膜蛋白(MIMP),具有抗炎功效,可显著缓解结肠炎模型小鼠的症状,并揭示了相关分子机制,或能用于炎症性肠病的临床治疗。相关成果在Cellular Physiology and Biochemistry发表,值得专业人士关注。
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Micro Integral Membrane Protein (MIMP), a Newly Discovered Anti-Inflammatory Protein of Lactobacillus Plantarum, Enhances the Gut Barrier and Modulates Microbiota and Inflammatory Cytokines

微整合膜蛋白(MIMP),一种新发现的植物乳杆菌抗炎蛋白,增强肠道屏障并调节菌群和炎性细胞因子

10.1159/000487027

2018-01-31, Article

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BACKGROUND/AIMS: Recent studies have demonstrated that the manipulation of the gut microbiome represents a promising treatment for inflammatory bowel disease (IBD). We previously identified micro integral membrane protein (MIMP) as the smallest domain of surface layer protein from Lactobacillus Plantarum. However, the therapeutic relevance of MIMP in IBD remains unknown.
METHODS: We initially employed a dextran sodium sulphate (DSS)-induced colitis model and evaluated the effect of MIMP on the inflammation response, intestinal barrier and gut microbiota using histological examination, Fluorescein isothiocyanate-Dextran detection and pyrosequencing analysis respectively. We then established peripheral blood mononuclear cells (PBMCs) and an epithelial CaCO-2 co-culture model to investigate the regulatory role of MIMP in inflammatory cytokines. The level changes of inflammatory cytokines were detected using Enzyme-linked immunosorbent and real-time polymerase chain reaction assay. The involved regulatory mechanisms were investigated mainly using dual luciferase reporter and chromatin immunoprecipitation assay.
RESULTS: In the DSS-induced colitis model, we observed that MIMP intervention effectively improved the body weight loss, increased the colon length and decreased disease activity index. Consistently, the inflammation scores in the MIMP treatment group were significantly lower than those in the DSS treatment group. Furthermore, MIMP intervention was found to successfully neutralize DSS treatment by decreasing the expression of pro-inflammatory cytokines (IFN-γ, IL-17 and IL-23) and increasing the expression of anti-inflammatory cytokines (IL-4 and IL-10). Notably, the permeability assay demonstrated that the MIMP treatment group was remarkably lower than that in the DSS treatment group. We also showed that MIMP improved gut microbiota dysbiosis caused by DSS-induced inflammation. Additionally, in PBMCs and the CaCO-2 co-culture model, MIMP showed an obvious suppressive effect on lipopolysaccharide-induced inflammation in a time- and dose-dependent manner. Furthermore, we revealed that MIMP could modulate inflammatory cytokine expression through the toll-like receptor 4 pathway and histone acetylation.
CONCLUSIONS: Our results suggested that MIMP showed a significant anti-inflammatory effect through regulating the gut barrier, microbiota and inflammatory cytokines. MIMP may have translational relevance as clinically relevant therapy for IBD patients.

First Authors:
Mingming Yin,Xuebing Yan,Wenhao Weng

Correspondence Authors:
Tongyi Shen,Yanlei Ma,Huanlong Qin

All Authors:
Mingming Yin,Xuebing Yan,Wenhao Weng,Yongzhi Yang,Renyuan Gao,Minfeng Liu,Cheng Pan,Qi Zhu,Hao Li,Qing Wei,Tongyi Shen,Yanlei Ma,Huanlong Qin

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