• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury
【24h】

Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury

机译：肾脏缺血再灌注损伤对肺过敏反应的调节

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The Th1/Th2 balance represents an important factor in the pathogenesis of renal ischemia-reperfusion injury (IRI). In addition, IRI causes a systemic inflammation that can affect other tissues, such as the lungs. To investigate the ability of renal IRI to modulate pulmonary function in a specific model of allergic inflammation, C57Bl/6 mice were immunized with ovalbumin/albumen on days 0 and 7 and challenged with an ovalbumin (OA) aerosol on days 14 and 21. After 24 h of the second antigen challenge, the animals were subjected to 45 minutes of ischemia. After 24 h of reperfusion, the bronchoalveolar lavage (BAL) fluid, blood and lung tissue were collected for analysis. Serum creatinine levels increased in both allergic and non-immunized animals subjected to IRI. However, BAL analysis showed a reduction in the total cells (46%) and neutrophils (58%) compared with control allergic animals not submitted to IRI. In addition, OA challenge induced the phosphorylation of ERK and Akt and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in lung homogenates. After renal IRI, the phosphorylation of ERK and expression of COX-2 and iNOS were markedly reduced; however, there was no difference in the phosphorylation of Akt between sham and ischemic OA-challenged animals. Mucus production was also reduced in allergic mice after renal IRI. IL-4, IL-5 and IL-13 were markedly down-regulated in immunized/challenged mice subjected to IRI. These results suggest that renal IRI can modulate lung allergic inflammation, probably by altering the Th1/Th2 balance and, at least in part, by changing cellular signal transduction factors.
机译：Th1 / Th2平衡是肾脏缺血再灌注损伤（IRI）发病机理的重要因素。此外，IRI引起全身性炎症，可能会影响其他组织，例如肺。为了研究在特定的过敏性炎症模型中肾脏IRI调节肺功能的能力，在第0天和第7天用卵清蛋白/白蛋白免疫C57Bl / 6小鼠，并在第14天和第21天用卵清蛋白（OA）气雾剂攻击。在第二次抗原攻击后24小时，使动物经历45分钟的局部缺血。再灌注24小时后，收集支气管肺泡灌洗液，血液和肺组织进行分析。接受IRI的过敏和未免疫动物的血清肌酐水平均升高。但是，BAL分析显示与未提交IRI的对照过敏性动物相比，总细胞（46％）和嗜中性粒细胞（58％）减少。此外，OA挑战诱导肺匀浆中ERK和Akt的磷酸化以及诱导型一氧化氮合酶（iNOS）和环氧合酶2（COX-2）的表达。肾IRI后，ERK的磷酸化以及COX-2和iNOS的表达显着降低。然而，在伪造和缺血性OA挑战动物之间，Akt的磷酸化没有差异。肾脏IRI后变态反应小鼠的粘液产生也减少。在接受IRI免疫/攻击的小鼠中，IL-4，IL-5和IL-13明显下调。这些结果表明，肾脏IRI可能通过改变Th1 / Th2平衡以及至少部分地通过改变细胞信号转导因子来调节肺部过敏性炎症。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号