...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Antibacterial Action of Extracellular Mammalian Group IIA Phospholipase A2 against Grossly ClumpedStaphylococcus aureus
【24h】

Antibacterial Action of Extracellular Mammalian Group IIA Phospholipase A2 against Grossly ClumpedStaphylococcus aureus

机译：细胞外哺乳动物IIA族磷脂酶A2对严重团聚的金黄色葡萄球菌的抗菌作用

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

摘要

Fibrinogen-dependent interactions of Staphylococcus aureus are believed to contribute to bacterial virulence by promoting bacterial attachment to fibrinogen-coated surfaces and inducing the formation of bacterial clumps that are likely resistant to phagocytosis. Although S. aureus produces several fibrinogen-binding proteins, the cell wall-associated protein clumping factor (encoded by clfA) appears to be most important in bacterial interactions with immobilized or soluble purified fibrinogen. We have compared bacterial clumping in several strains of S. aureus, including isogenic ClfA+ and ClfA? Newman strains, in the presence of purified rabbit fibrinogen, human plasma, and inflammatory fluid and examined the effect of clumping on bacterial sensitivity to mammalian group IIA phospholipase A2 (PLA2). This enzyme is the major extracellular bactericidal agent in inflammatory fluid active against S. aureus. Both ClfA-dependent and ClfA-independent bacterial clumping was observed, depending on the source and fibrinogen content of the biological fluid. In each case, clumping only partially reduced the antibacterial activity of PLA2, suggesting that this extracellular enzyme can substantially penetrate dense bacterial clumps. Bacterial clumps could be dispersed by added proteases, restoring full antibacterial activity to PLA2. Thus, the extracellular mobilization of group IIA PLA2 during inflammation may provide a mechanism by which the host can control the proliferation and survival of S. aureus even after bacterial clumping.
机译：据信金黄色葡萄球菌的纤维蛋白原依赖性相互作用通过促进细菌附着到纤维蛋白原包被的表面上并诱导可能抗吞噬作用的细菌团块的形成而导致细菌毒力。虽然 S。金黄色葡萄球菌产生几种纤维蛋白原结合蛋白，细胞壁相关蛋白聚集因子（由 clfA 编码）在固定化或可溶性纯化的纤维蛋白原的细菌相互作用中似乎最重要。我们比较了几种 S菌株中的细菌结块。在纯化的兔纤维蛋白原，人血浆和炎性液体存在下，包括同基因的ClfA + 和ClfA ？ Newman菌株的金黄色葡萄球菌，并研究了结块的作用对细菌对哺乳动物IIA组磷脂酶A2（PLA2）的敏感性。该酶是对 S有活性的炎性液体中的主要细胞外杀菌剂。金黄色。取决于生物流体的来源和纤维蛋白原含量，都观察到了ClfA依赖性和ClfA依赖性细菌团块。在每种情况下，团块仅部分降低了PLA2的抗菌活性，表明该细胞外酶可以充分穿透致密的细菌团块。细菌团块可以通过添加蛋白酶分散，从而恢复对PLA2的完全抗菌活性。因此，炎症过程中IIA PLA2组的细胞外动员可能提供一种机制，宿主可以通过该机制控制 S的增殖和存活。甚至在细菌结块后仍保持金黄色。

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