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首页> 外文期刊>World Journal of Gastroenterology >Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice
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Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice

机译：氯化钠通过p38 / MAPK途径调节小鼠的促炎和抗炎固有层固有核细胞，加剧了葡聚糖硫酸钠引起的结肠炎

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AIM To investigate the influence of high salt on dextran sulfate sodium (DSS)-induced colitis in mice and explore the underlying mechanisms of this effect. METHODS DSS and NaCl were used to establish the proinflammatory animal model. We evaluated the colitis severity. Flow cytometry was employed for detecting the frequencies of Th1, macrophages and Tregs in spleen, mesenteric lymph node and lamina propria. The important role of macrophages in the promotion of DSS-induced colitis by NaCl was evaluated by depleting macrophages with clodronate liposomes. Activated peritoneal macrophages and lamina propria mononuclear cells (LPMCs) were stimulated with NaCl, and proteins were detected by western blotting. Cytokines and inflammation genes were analyzed by enzyme-linked immunosorbent assay and RT-PCR, respectively. RESULTS The study findings indicate that NaCl up-regulates the frequencies of CD11b+ macrophages and CD4+IFN-γ+IL-17+ T cells in lamina propria in DSS-treated mice. CD3+CD4+CD25+Foxp3+ T cells, which can secrete high levels of IL-10 and TGF-β, increase through feedback in NaCl- and DSS-treated mice. Furthermore, clodronate liposomes pretreatment significantly alleviated DSS-induced colitis, indicating that macrophages play a vital role in NaCl proinflammatory activity. NaCl aggravates peritoneal macrophage inflammation by promoting the expressions of interleukin (IL)-1, IL-6 and mouse inducible nitric oxide synthase. Specifically, high NaCl concentrations promote p38 phosphorylation in lipopolysaccharide- and IFN-γ-activated LPMCs mediated by SGK1. CONCLUSION Proinflammatory macrophages may play an essential role in the onset and development of NaCl-promoted inflammation in DSS-induced colitis. The underlining mechanism involves up-regulation of the p38/MAPK axis.
机译：目的研究高盐对小鼠右旋糖酐硫酸钠（DSS）引起的结肠炎的影响，并探讨其作用机理。方法采用DSS和NaCl建立促炎动物模型。我们评估了结肠炎的严重程度。流式细胞仪用于检测脾脏，肠系膜淋巴结和固有层中Th1，巨噬细胞和Treg的频率。通过用氯膦酸盐脂质体消耗巨噬细胞来评估巨噬细胞在NaCl促进DSS诱导的结肠炎中的重要作用。用氯化钠刺激活化的腹膜巨噬细胞和固有层单核细胞（LPMC），并通过蛋白质印迹法检测蛋白质。分别通过酶联免疫吸附测定和RT-PCR分析细胞因子和炎症基因。结果研究结果表明，NaCl上调CD11b + 巨噬细胞和CD4 + IFN-γ + IL-17 的频率DSS处理过的小鼠固有层中的+ T细胞。 CD3 + CD4 + CD25 + Foxp3 + T细胞，它们可以分泌高水平的IL-10和TGF -β通过NaCl和DSS处理的小鼠的反馈而增加。此外，氯膦酸盐脂质体预处理可显着缓解DSS诱导的结肠炎，表明巨噬细胞在NaCl促炎活性中起着至关重要的作用。 NaCl通过促进白介素（IL）-1，IL-6和小鼠诱导型一氧化氮合酶的表达来加重腹膜巨噬细胞炎症。具体而言，高NaCl浓度可促进SGK1介导的脂多糖和IFN-γ激活的LPMC中的p38磷酸化。结论促炎性巨噬细胞可能在DSS诱发的结肠炎中NaCl促进的炎症的发生和发展中起重要作用。强调机制涉及p38 / MAPK轴的上调。

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