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首页> 外文期刊>Cellular Physiology and Biochemistry >Inflammasome Activation by ATP Enhances Citrobacter rodentium Clearance through ROS Generation
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Inflammasome Activation by ATP Enhances Citrobacter rodentium Clearance through ROS Generation

机译：ATP激活炎症小体通过产生ROS增强柠檬酸杆菌的清除率

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>Background: Nod-like receptor family, pyrin domain containing 3 (NLRP3) is an important cytosolic sensor of cellular stress and infection. Once activated, NLRP3 forms a multiprotein complex (inflammasome) that triggers the maturation and secretion of interleukin (IL)-1?2 and IL-18. We aimed to define the consequences of NLRP3 induction, utilizing exogenous adenosine triphosphate (ATP) as an inflammasome activator, to determine if inflammasome activation increases macrophage killing of Citrobacter rodentium and define mechanisms. Methods: Bacterial survival was measured using a gentamicin protection assay. Inflammasome activation or inhibition in mouse J774A.1 macrophages were assessed by measuring IL-1?2; cytokines and reactive oxygen species (ROS) were measured by ELISA and DCFDA, respectively. Results: Activation of the inflammasome increased bacterial killing by macrophages and its inhibition attenuated this effect with no impact on phagocytosis or cell death. Furthermore, inflammasome activation suppressed pro-inflammatory cytokines during infection, possibly due to more effective bacterial killing. While the infection increased ROS production, this effect was reduced by inflammasome inhibitors, indicating that ROS is inflammasome-dependent. ROS inhibitors increased bacterial survival in the presence of ATP, suggesting that inflammasome-induced bacterial killing is mediated, at least in part, by ROS activity. Conclusion: Improving inflammasome activity during infection may increase bacterial clearance by macrophages and reduce subsequent microbe-induced inflammation.
机译：> 背景： 类似于Nod的受体家族，含3的吡啶结构域（NLRP3）是细胞应激和感染的重要胞质传感器。一旦激活，NLRP3就会形成一种多蛋白复合物（炎性体），触发白介素（IL）-1？2和IL-18的成熟和分泌。我们旨在通过利用外源三磷酸腺苷（ATP）作为炎性体激活剂来确定NLRP3诱导的后果，以确定炎性体激活是否会增加啮齿类柠檬酸杆菌的巨噬细胞杀伤率并确定机制。 方法： 使用庆大霉素保护试验测定细菌存活率。通过测量IL-1β2评估小鼠J774A.1巨噬细胞中的炎性体激活或抑制。分别通过ELISA和DCFDA测量细胞因子和活性氧（ROS）。 结果： 炎性小体的激活增加了巨噬细胞对细菌的杀灭作用，其抑制作用减弱了这种作用，而对吞噬作用或细胞死亡没有影响。此外，炎症小体的活化抑制了感染期间的促炎细胞因子，这可能是由于更有效的细菌杀伤作用所致。尽管感染增加了ROS的产生，但炎性体抑制剂抑制了这种作用，表明ROS是炎性体依赖性的。 ROS抑制剂在存在ATP的情况下提高了细菌的存活率，这表明炎症小体诱导的细菌杀伤至少部分是由ROS活性介导的。 结论： 在感染过程中改善炎症小体活性可能会增加巨噬细胞对细菌的清除率，并减少随后的微生物诱发的炎症。

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