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首页> 外文期刊>American Journal of Physiology >Downregulation of migration inhibitory factor is critical for estrogen-mediated attenuation of lung tissue damage following trauma-hemorrhage.
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Downregulation of migration inhibitory factor is critical for estrogen-mediated attenuation of lung tissue damage following trauma-hemorrhage.

机译：迁移抑制因子的下调对于外伤性出血后雌激素介导的肺组织损伤的减轻至关重要。

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Although studies have shown that 17beta-estradiol (E(2)) prevents neutrophil infiltration and organ damage following trauma-hemorrhage, the mechanism by which E(2) inhibits neutrophil transmigration remains unknown. Macrophage migration inhibitory factor (MIF) is thought to play a central role in exacerbation of inflammation and is associated with lung injury. MIF regulates the inflammatory response through modulation of Toll-like receptor 4 (TLR4). Activation of TLR4 results in the release of proinflammatory cytokines and chemokines, which induce neutrophil infiltration and subsequent tissue damage. We hypothesized that E(2) mediates its salutary effects in the lung following trauma-hemorrhage via negative regulation of MIF and modulation of TLR4 and cytokine-induced chemotaxis. C3H/HeOuJ mice were subjected to trauma-hemorrhage (mean blood pressure 35 +/- 5 mmHg for approximately 90 min, then resuscitation) or sham operation. Mice received vehicle, E(2), or E(2) in combination with recombinant mouse MIF protein (rMIF). Trauma-hemorrhage increased lung MIF and TLR4 protein levels as well as lung and systemic levels of cytokines/chemokines. Treatment of animals with E(2) following trauma-hemorrhage prevented these changes. However, administration of rMIF protein with E(2) abolished the E(2)-mediated decrease in lung TLR4 levels, lung and plasma levels of IL-6, TNF-alpha, monocyte chemoattractant protein-1, and keratinocyte-derived chemokine (KC). Administration of rMIF protein also prevented E(2)-mediated reduction in neutrophil influx and tissue damage in the lungs following trauma-hemorrhage. These results suggest that the protective effects of E(2) on lung injury following trauma-hemorrhage are mediated via downregulation of lung MIF and TLR4-induced cytokine/chemokine production.
机译：尽管研究表明17β-雌二醇（E（2））可以防止中性粒细胞浸润和创伤性出血后器官损伤，但E（2）抑制中性粒细胞转运的机制仍然未知。巨噬细胞迁移抑制因子（MIF）被认为在炎症加重中起核心作用，并与肺损伤有关。 MIF通过调节Toll样受体4（TLR4）调节炎症反应。 TLR4的激活导致促炎细胞因子和趋化因子的释放，从而诱导中性粒细胞浸润和随后的组织损伤。我们假设E（2）通过MIF的负调节和TLR4的调节以及细胞因子诱导的趋化性在创伤性出血后在肺中介导其有益作用。使C3H / HeOuJ小鼠遭受外伤性出血（平均血压35 +/- 5 mmHg，持续约90分钟，然后进行复苏）或假手术。小鼠接受了载体，E（2）或E（2）与重组小鼠MIF蛋白（rMIF）的结合。创伤出血增加了肺MIF和TLR4蛋白水平以及肺和全身细胞因子/趋化因子的水平。创伤出血后用E（2）处理动物可防止这些变化。但是，将rMIF蛋白与E（2）一起使用可消除E（2）介导的肺TLR4水平，肺和血浆IL-6，TNF-α，单核细胞趋化蛋白1和角质形成细胞趋化因子的降低（ KC）。 rMIF蛋白的管理还可以防止创伤性出血后E（2）介导的中性粒细胞流入减少和肺组织损伤。这些结果表明，E（2）对创伤性出血后肺损伤的保护作用是通过下调肺MIF和TLR4诱导的细胞因子/趋化因子产生而介导的。

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