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首页> 外文期刊>Infection and immunity >Monocyte Chemoattractant Protein 1, Macrophage Inflammatory Protein 1α, and RANTES Recruit Macrophages to the Kidney in a Mouse Model of Hemolytic-Uremic Syndrome
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Monocyte Chemoattractant Protein 1, Macrophage Inflammatory Protein 1α, and RANTES Recruit Macrophages to the Kidney in a Mouse Model of Hemolytic-Uremic Syndrome

机译：在溶血性尿毒症综合征小鼠模型中，单核细胞趋化蛋白1，巨噬细胞炎性蛋白1α和RANTES招募肾巨噬细胞。

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The macrophage has previously been implicated in contributing to the renal inflammation associated with hemolytic-uremic syndrome (HUS). However, there is currently no in vivo model detailing the contribution of the renal macrophage to the kidney disease associated with HUS. Therefore, renal macrophage recruitment and inhibition of infiltrating renal macrophages were evaluated in an established HUS mouse model. Macrophage recruitment to the kidney was evident by immunohistochemistry 2 h after administration of purified Stx2 and peaked at 48 h postinjection. Mice administered a combination of Stx2 and lipopolysaccharide (LPS) showed increased macrophage recruitment to the kidney compared to mice treated with Stx2 or LPS alone. Monocyte chemoattractants were induced in the kidney, including monocyte chemoattractant protein 1 (MCP-1/CCL2), macrophage inflammatory protein 1α (MIP-1α/CCL3), and RANTES (CCL5), in a pattern that was coincident with macrophage infiltration as indicated by immunohistochemistry, protein, and RNA analyses. MCP-1 was the most abundant chemokine, MIP-1α was the least abundant, and RANTES levels were intermediate. Mice treated with MCP-1, MIP-1α, and RANTES neutralizing antibodies had a significant decrease in Stx2 plus LPS-induced macrophage accumulation in the kidney, indicating that these chemokines are required for macrophage recruitment. Furthermore, mice exposed to these three neutralizing antibodies had decreased fibrin deposition in their kidneys, implying that macrophages contribute to the renal damage associated with HUS.
机译：先前已经证明巨噬细胞参与与溶血尿毒症综合征（HUS）有关的肾脏炎症。但是，目前尚无体内模型详细说明肾巨噬细胞对与HUS相关的肾脏疾病的贡献。因此，在建立的HUS小鼠模型中评估了肾巨噬细胞募集和对浸润性肾巨噬细胞的抑制。给予纯化的Stx2 2小时后，免疫组织化学证实巨噬细胞募集至肾脏，并在注射后48 h达到峰值。与单独使用Stx2或LPS处理的小鼠相比，与Stx2和脂多糖（LPS）组合使用的小鼠显示出巨噬细胞向肾脏的募集。在肾脏中诱导了单核细胞趋化因子，包括单核细胞趋化因子蛋白1（MCP-1 / CCL2），巨噬细胞炎性蛋白1α（MIP-1α/ CCL3）和RANTES（CCL5），其模式与巨噬细胞浸润一致通过免疫组织化学，蛋白质和RNA分析。 MCP-1是最丰富的趋化因子，MIP-1α是最不丰富的趋化因子，而RANTES水平是中等的。用MCP-1，MIP-1α和RANTES中和抗体治疗的小鼠肾脏中Stx2加LPS诱导的巨噬细胞蓄积量显着减少，表明这些趋化因子是募集巨噬细胞所必需的。此外，暴露于这三种中和抗体的小鼠肾脏纤维蛋白沉积减少，这表明巨噬细胞有助于与HUS相关的肾脏损害。

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