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Research Article Inhalative IL-10 Attenuates Pulmonary Inflammation following Hemorrhagic Shock without Major Alterations of the Systemic Inflammatory Response

机译:研究文章吸入性IL-10可减轻失血性休克后的肺部炎症,而不会引起全身炎症反应的重大改变

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Several studies report immunomodulatory effects of endogenous IL-10 after trauma. The present study investigates the effect of inhalative IL-10 administration on systemic and pulmonary inflammation in hemorrhagic shock. Male C57/BL6 mice (8 animals per group) were subjected to pressure-controlled hemorrhagic shock for 1.5 hrs followed by resuscitation and inhalative administration of either 50 muL PBS (Shock group) or 50mug/kg recombinant mouse IL-10 dissolved in 50 muL PBS (Shock + IL-10 group). Animals were sacrificed after 4.5 hrs of recovery and serum IL-6, IL-10, KC, and MCP-1 concentrations were measured with ELISA kits. Acute pulmonary inflammation was assessed by pulmonary myeloperoxidase (MPO) activity and pulmonary H&E histopathology. Inhalative IL-10 administration decreased pulmonary inflammation without altering the systemic concentrations of IL-6, IL-10, and KC. Serum MCP-1 levels were significantly reduced following inhalative IL-10 administration. These findings suggest that inhalative IL-10 administration may modulate the pulmonary microenvironment without major alterations of the systemic inflammatory response, thus minimizing the potential susceptibility to infection and sepsis.
机译:几项研究报道了创伤后内源性IL-10的免疫调节作用。本研究调查了失血性休克中吸入IL-10对全身和肺部炎症的影响。对雄性C57 / BL6小鼠(每组8只动物)进行压力控制的失血性休克1.5小时,然后复苏并吸入溶解在50μL的50μLPBS(休克组)或50μg/ kg的重组小鼠IL-10 PBS(Shock + IL-10组)。恢复4.5小时后处死动物,并用ELISA试剂盒测量血清IL-6,IL-10,KC和MCP-1浓度。通过肺髓过氧化物酶(MPO)活性和肺H&E组织病理学评估急性肺炎症。吸入性IL-10给药可减少肺部炎症,而不会改变IL-6,IL-10和KC的全身浓度。吸入IL-10后,血清MCP-1水平显着降低。这些发现表明,吸入性IL-10的给药可以调节肺微环境,而不会引起全身性炎症反应的重大改变,从而使对感染和败血症的潜在易感性降至最低。

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