Mannose-capped lipoarabinomannan-induced B10 cells decrease severity of dextran sodium sulfate-induced inflammatory bowel disease in mice.
Mannose-capped lipoarabinomannan-induced B10 cells decrease severity of dextran sodium sulfate-induced inflammatory bowel disease in mice.
复制标题
甘露糖封端的阿拉伯脂甘露聚糖诱导的 B10 细胞可降低右旋糖酐硫酸钠诱导的小鼠炎症性肠病的严重程度。
DOI：
10.1111/sji.12843
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发表时间：
2019
影响因子：
3.7
通讯作者：
Pan Qin
中科院分区：
文献类型：
--
作者：
Yuan Chunhui;Li Xin;Luo Liang;Wang Yaping;Zhang Dongli;Zhou Kai Liang;Zhang Xiao-Lian;Pan Qin
炎症性肠病（IBD）是一种慢性、非特异性、炎症性胃肠道疾病，主要由克罗恩病和溃疡性结肠炎组成。然而，IBD的病因和发病机制仍不清楚。已知B10（产生IL-10的调节性B）细胞是调节性B细胞的一个亚群，有助于肠道内稳态，B10细胞的异常频率与IBD相关。我们最近报道了B10细胞可以被ManLAM（甘露糖帽脂阿拉伯甘露聚糖）诱导，ManLAM是结核分枝杆菌（Mycobacterium tuberculosis）的主要细胞壁脂聚糖。在本研究中，将ManLAM诱导的B10细胞过继转移至IL（白细胞介素）-10 −/−小鼠中，并在DSS（葡聚糖硫酸钠）诱导的IBD模型中研究了ManLAM诱导的B10细胞的作用。ManLAM诱导的B10细胞降低小鼠结肠炎的严重程度。B10细胞下调DSS处理小鼠脾脏和MLN（肠系膜淋巴结）中的Th 1极化。这些结果表明，ManLAM处理的B细胞产生的IL-10有助于保持CD 4 +T细胞亚群之间的平衡，并保护小鼠免受DSS诱导的IBD。
Inflammatory bowel disease (IBD) is a chronic, non‐specific, inflammatory gastrointestinal disease that mainly consists of Crohn's disease and ulcerative colitis. However, the aetiology and pathogenesis of IBD are still unclear. B10 (IL‐10 producing regulatory B) cells, a subset of regulatory B cells, are known to contribute to intestinal homeostasis and the aberrant frequency of B10 cells is associated with IBD. We have recently reported that B10 cells can be induced by ManLAM (mannose‐capped lipoarabinomannan), a major cell‐wall lipoglycan ofM tb(Mycobacterium tuberculosis). In the current study, the ManLAM‐induced B10 cells were adoptively transferred into IL(interleukin)‐10−/−mice and the roles of ManLAM‐induced B10 cells were investigated in DSS (dextran sodium sulphate)‐induced IBD model. ManLAM‐induced B10 cells decrease colitis severity in the mice. The B10 cells downregulate Th1 polarization in spleen and MLNs (mesenteric lymph nodes) of DSS‐treated mice. These results suggest that IL‐10 production by ManLAM‐treated B cells contributes to keeping the balance between CD4+T cell subsets and protect mice from DSS‐induced IBD.