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首页> 外文期刊>American Journal of Physiology >Involvement of high mobility group box 1 in the pathogenesis of severe hemolytic uremic syndrome in a murine model.
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Involvement of high mobility group box 1 in the pathogenesis of severe hemolytic uremic syndrome in a murine model.

机译：高迁移率组箱1在鼠模型中严重溶血性尿毒综合征的发病机制。

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摘要

Typical hemolytic uremic syndrome is caused by Shiga toxin (Stx2) and lipopolysaccharide (LPS) of Escherichia coli and leads to acute kidney injury. The role of innate immunity in this pathogenesis is unclear. We analyzed the role of high mobility group box 1 (HMGB1) at the onset of disease in a murine model. C57BL/6 mice were intraperitoneally administered saline {group A), anti-HMGB1 monoclonal antibody (group B), Stx2 and LPS to elicit severe disease (group C), or Stx2, LPS, and anti-HMGB1 antibody (group D). While all mice in group C died by day 5 of the experiment, all mice in group D survived. Anemia and thrombocytopenia were pronounced and plasma creatinine levels were significantly elevated in group C only at 72 h. While at 72 h after toxin administration the glomerulus tissue in group C showed pathology similar to that of humans, mesangial cell proliferation was seen in group D. Plasma HMGB1 levels in group C peaked 3 h after administration and were higher than those in other groups. Expression of the receptor of advanced glycation end products and NF-kB, involved in HMGB1 signaling, was significantly elevated in group C but not in group D. Administration of anti-HMGBl antibody in a murine model of severe disease inhibited plasma HMGB1 and promoted amelioration of tissue damage. HMGB1 was found to be involved in the disease pathology; therefore, controlling HMGB1 activity might inhibit disease progression.
机译：典型的溶血性尿性综合征是由大肠杆菌的Shiga毒素（STX2）和脂多糖（LPS）引起的，导致急性肾损伤。先天免疫在这种发病机制中的作用尚不清楚。我们分析了高迁移率组箱1（HMGB1）在鼠模型中疾病发作的作用。 C57BL / 6小鼠腹膜内施用盐水{组A），抗HMGB1单克隆抗体（B），STX2和LPS，以引发严重的疾病（C），或STX2，LPS和抗HMGB1抗体（D组D）。虽然C组中的所有小鼠在实验的第5天死亡时，D组的所有小鼠都存活下来。贫血和血小板减少症在72小时内仅在C组中显着升高。虽然在毒素施用后72小时，C组中的肾小球组织显示出类似的病理学类似于人类的病理学，但在施用后，C组中的血浆HMGB1水平达到3小时，并高于其他组的血浆HMGB1水平。 C组的晚期糖化末端产物和NF-KB的受体的表达在C组中显着升高，但在D.抗HMGBL抗体施用严重疾病中的抗HMGBL抗体抑制血浆模型抑制血浆HMGB1，促进改善组织损伤。发现HMGB1参与疾病病理;因此，控制HMGB1活性可能会抑制疾病进展。

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