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首页> 外文期刊>Infection and immunity >Dietary Glycine Prevents Peptidoglycan Polysaccharide-Induced Reactive Arthritis in the Rat: Role for Glycine-Gated Chloride Channel
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Dietary Glycine Prevents Peptidoglycan Polysaccharide-Induced Reactive Arthritis in the Rat: Role for Glycine-Gated Chloride Channel

机译：膳食甘氨酸预防大鼠中肽聚糖多糖诱导的反应性关节炎：甘氨酸门控氯离子通道的作用

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Peptidoglycan polysaccharide (PG-PS) is a primary structural component of bacterial cell walls and causes rheumatoid-like arthritis in rats. Recently, glycine has been shown to be a potential immunomodulator; therefore, the purpose of this study was to determine if glycine would be protective in a PG-PS model of arthritis in vivo. In rats injected with PG-PS intra-articularly, ankle swelling increased 21% in 24 to 48 h and recovered in about 2 weeks. Three days prior to reactivation with PG-PS given intravenously (i.v.), rats were divided into two groups and fed a glycine-containing or nitrogen-balanced control diet. After i.v. PG-PS treatment joint swelling increased 2.1 ± 0.3 mm in controls but only 1.0 ± 0.2 mm in rats fed glycine. Infiltration of inflammatory cells, edema, and synovial hyperplasia in the joint were significantly attenuated by dietary glycine. Tumor necrosis factor alpha (TNF-α) mRNA was detected in ankle homogenates from rats fed the control diet but not in ankles from rats fed glycine. Moreover, intracellular calcium was increased significantly in splenic macrophages treated with PG-PS; however, glycine blunted the increase about 50%. The inhibitory effect of glycine was reversed by low concentrations of strychnine or chloride-free buffer, and it increased radiolabeled chloride influx nearly fourfold, an effect also inhibited by strychnine. In isolated splenic macrophages, glycine blunted translocation of the p65 subunit of NF-κB into the nucleus, superoxide generation, and TNF-α production caused by PG-PS. Further, mRNA for the beta subunit of the glycine receptor was detected in splenic macrophages. This work supports the hypothesis that glycine prevents reactive arthritis by blunting cytokine release from macrophages by increasing chloride influx via a glycine-gated chloride channel.
机译：肽聚糖多糖（PG-PS）是细菌细胞壁的主要结构成分，可引起大鼠类风湿样关节炎。最近，甘氨酸已被证明是一种潜在的免疫调节剂。因此，本研究的目的是确定甘氨酸在体内PG-PS关节炎模型中是否具有保护作用。在关节内注射PG-PS的大鼠中，踝关节肿胀在24至48小时内增加了21％，并在约2周内恢复。静脉内（i.v.）给予PG-PS激活前三天，将大鼠分为两组，并饲喂含甘氨酸或氮平衡的对照饮食。在i.v.之后PG-PS处理的关节肿胀在对照组中增加2.1±0.3 mm，但在饲喂甘氨酸的大鼠中仅增加1.0±0.2 mm。饮食中的甘氨酸可明显减轻关节中炎性细胞的浸润，水肿和滑膜增生。在饲喂对照饮食的大鼠的踝匀浆中检测到肿瘤坏死因子α（TNF-α）mRNA，但在饲喂甘氨酸的大鼠的踝部中未检测到。此外，PG-PS处理的脾巨噬细胞中的细胞内钙显着增加。但是，甘氨酸抑制了约50％的增加。甘氨酸的抑制作用被低浓度的士的宁或不含氯的缓冲液逆转，它使放射性标记的氯离子流入增加了近四倍，该作用也被士的宁抑制。在孤立的脾脏巨噬细胞中，甘氨酸抑制了PG-PS引起的NF-κBp65亚基向核内的移位，超氧化物的产生和TNF-α的产生。此外，在脾巨噬细胞中检测到甘氨酸受体β亚基的mRNA。这项工作支持以下假设：甘氨酸通过通过甘氨酸门控氯化物通道增加氯化物流入，使巨噬细胞释放的细胞因子钝化，从而预防了反应性关节炎。

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