...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Role of Pseudomonas aeruginosa lipase in inflammatory mediator release from human inflammatory effector cells (platelets, granulocytes, and monocytes.
【24h】

Role of Pseudomonas aeruginosa lipase in inflammatory mediator release from human inflammatory effector cells (platelets, granulocytes, and monocytes.

机译：铜绿假单胞菌脂肪酶在人类炎症效应细胞（血小板，粒细胞和单核细胞）释放炎症介质中的作用。

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

摘要

Previously, we have shown that Pseudomonas aeruginosa lipase and phospholipase C (PLC), two extracellular lipolytic enzymes, interact with each other during 12-hydroxyeicosatetraenoic acid (HETE) generation from human platelets. In this regard. the addition of purified P. aeruginosa lipase to PLC-containing crude P. aeruginosa culture supernatants enhances the generation of the chemotactically active 12-HETE from human platelets. Therefore, we analyzed the interaction of purified P. aeruginosa lipase and purified hemolytic P. aeruginosa PLC with regard to inflammatory mediator release from human platelets, neutrophilic and basophilic granulocytes, and monocytes. Purified P. aeruginosa PLC, but not purified lipase by itself, induced 12-HETE generation from human platelets, the generation of leukotriene B4 (LTB4) and oxygen metabolites, enzyme release from human neutrophils, and histamine release from basophils but diminished interleukin-8 (IL-8) release from human monocytes in a dose-dependent manner. The addition of purified lipase enhanced PLC-induced 12-HETE and LTB4 generation, did not influence enzyme, histamine, or IL-8 release, but diminished the PLC-induced chemiluminescent response. Similar results were obtained when the hemolytic PLC from Clostridium perfringens was used instead of P. aeruginosa PLC. For further comparison, we used the well-defined calcium ionophore A23187 and phorbol-12-myristate-13-acetate (PMA) as stimuli. Lipase enhanced calcium ionophore-induced LTB4 generation and beta-glucuronidase release but reduced calcium ionophore-induced and PMA-induced chemiluminescence. In parallel, we analyzed the role of lipase in a crude P. aeruginosa culture supernatant containing PLC and lipase. Lipase activity in the P. aeruginosa culture supernatant was inhibited by treatment with the lipase-specific inhibitor hexadecylsulfonyl fluoride, leaving the activity of PLC unaffected. The capacity of "lipase-inactivated culture supernatant" to induce 12-HETE and LTB4 generation was diminished by 50 to 100%. Our results suggest that the simultaneous secretion of lipase and PLC by P. aeruginosa residing in an infected host may result in severe pathological effects which cannot be explained by the sole action of the individual virulence factor on inflammatory effector cells.
机译：以前，我们已经显示了铜绿假单胞菌脂肪酶和磷脂酶C（PLC），两种细胞外脂解酶，在从人血小板生成12-羟基二十碳四烯酸（HETE）的过程中彼此相互作用。在这方面。向含有PLC的粗铜绿假单胞菌培养上清液中添加纯化的铜绿假单胞菌脂肪酶可增强人血小板产生趋化活性12-HETE的能力。因此，我们分析了纯化的铜绿假单胞菌脂肪酶和纯化的溶血性铜绿假单胞菌PLC在人血小板，嗜中性和嗜碱性粒细胞以及单核细胞中炎症介质释放方面的相互作用。纯化的铜绿假单胞菌PLC本身而非纯化的脂肪酶可诱导人血小板产生12-HETE，白三烯B4（LTB4）和氧代谢产物，人嗜中性粒细胞释放酶，嗜碱性粒细胞释放组胺，但白介素8减少（IL-8）以剂量依赖性方式从人单核细胞释放。纯化的脂肪酶的添加增强了PLC诱导的12-HETE和LTB4的生成，但不影响酶，组胺或IL-8的释放，但减少了PLC诱导的化学发光反应。当使用来自产气荚膜梭菌的溶血性PLC代替铜绿假单胞菌PLC时，获得了相似的结果。为了进行进一步的比较，我们使用定义明确的钙离子载体A23187和佛波12-肉豆蔻酸13-醋酸酯（PMA）作为刺激。脂肪酶增强了钙离子载体诱导的LTB4生成和β-葡萄糖醛酸苷酶的释放，但降低了钙离子载体诱导的和PMA诱导的化学发光。同时，我们分析了脂肪酶在含有PLC和脂肪酶的粗铜绿假单胞菌培养上清液中的作用。铜绿假单胞菌培养上清中的脂肪酶活性通过用脂肪酶特异性抑制剂十六烷基磺酰氟处理而受到抑制，而PLC的活性不受影响。 “脂肪酶灭活的培养上清液”诱导12-HETE和LTB4产生的能力降低了50％至100％。我们的结果表明，驻留在被感染宿主中的铜绿假单胞菌同时分泌脂肪酶和PLC可能导致严重的病理学效应，这不能通过单个毒力因子对炎症效应细胞的单独作用来解释。

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