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首页> 外文期刊>Journal of Cellular Physiology >Platelet-Derived CCL5 Regulates CXC Chemokine Formation and Neutrophil Recruitment in Acute Experimental Colitis
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Platelet-Derived CCL5 Regulates CXC Chemokine Formation and Neutrophil Recruitment in Acute Experimental Colitis

机译：血小板源CCL5调节科学家趋化因子形成和嗜中性粒细胞在急性招聘实验性结肠炎

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Accumulating data suggest that platelets not only regulate thrombosis and haemostasis but also inflammatory processes. Platelets contain numerous potent pro-inflammatory compounds, including the chemokines CCL5 and CXCL4, although their role in acute colitis remains elusive. The aim of this study is to examine the role of platelets and platelet-derived chemokines in acute colitis. Acute colitis is induced in female Balb/c mice by administration of 5% dextran sodium sulfate (DSS) for 5 days. Animals receive a platelet-depleting, anti-CCL5, anti-CXCL4, or a control antibody prior to DSS challenge. Colonic tissue is collected for quantification of myeloperoxidase (MPO) activity, CXCL5, CXCL2, interleukin-6 (IL-6), and CCL5 levels as well as morphological analyses. Platelet depletion reduce tissue damage and clinical disease activity index in DSS-exposed animals. Platelet depletion not only reduces levels of CXCL2 and CXCL5 but also levels of CCL5 in the inflamed colon. Immunoneutralization of CCL5 but not CXCL4 reduces tissue damage, CXC chemokine expression, and neutrophil recruitment in DSS-treated animals. These findings show that platelets play a key role in acute colitis by regulating CXC chemokine generation, neutrophil infiltration, and tissue damage in the colon. Moreover, our results suggest that platelet-derived CCL5 is an important link between platelet activation and neutrophil recruitment in acute colitis. J. Cell. Physiol. 231: 370-376, 2016. (c) 2015 Wiley Periodicals, Inc.
机译：积累的数据表明,血小板不仅调节血栓和止血炎症过程。许多有效的促炎症化合物,包括趋化因子CCL5 CXCL4,虽然他们的角色在急性结肠炎仍然遥遥无期。本研究的目的是检查的作用血小板和血小板源趋化因子急性结肠炎。Balb / c小鼠5%右旋糖酐的政府硫酸钠(DSS)为5天。platelet-depleting、anti-CCL5 anti-CXCL4或控制抗体之前DSS的挑战。组织收集的量化髓过氧化酶(MPO)活动,CXCL5 CXCL2,白细胞介素- 6 (il - 6),以及CCL5水平形态分析。组织损伤和临床疾病活动指数在DSS-exposed动物。只有CXCL2水平降低和CXCL5也在结肠发炎CCL5水平。Immunoneutralization CCL5但不是CXCL4减少组织损伤,科学家趋化因子表达式,并在DSS-treated中性粒细胞招募动物。一个关键的角色在急性结肠炎通过调节科学家趋化因子生成、嗜中性粒细胞浸润并在结肠组织损伤。结果表明,血小板源CCL5是一个血小板激活和之间重要的联系中性粒细胞招募在急性结肠炎。杂志。231:370 - 376年,2016年。期刊、公司。

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