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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >α-hemolysin From Eschehchia Coli Uses Endogenous Amplification Through P2x Receptor Activation To Induce Hemolysis
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α-hemolysin From Eschehchia Coli Uses Endogenous Amplification Through P2x Receptor Activation To Induce Hemolysis

机译：大肠杆菌中的α-溶血素通过P2x受体激活利用内源性扩增诱导溶血

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摘要

Escherichia coli is the dominant facultative bacterium in the normal intestinal flora. E. coli is, however, also responsible for the majority of serious extraintestinal infections. There are distinct serotypical differences between facultative and invasive E. coli strains. Invasive strains frequently produce virulence factors such as α-hemolysin (HlyA), which causes hemolysis by forming pores in the erythrocyte membrane. The present study reveals that this pore formation triggers purinergic receptor activation to mediate the full hemo-lytic action. Non-selective ATP-receptor (P2) antagonists (PPADS, suramin) and ATP scavengers (apyrase, hexokinase) concentration dependently inhibited HlyA-induced lysis of equine, murine, and human erythrocytes. The pattern of responsiveness to more selective P2-antagonists implies that both P2X_1 and P2X_7 receptors are involved in HlyA-induced hemolysis in all three species. In addition, our results also propose a role for the pore protein pannexin1 in HlyA-induced hemolysis, as non-selective inhibitors of this channel significantly reduced hemolysis in the three species. In conclusion, activation of P2X receptors and possibly also pannexins augment hemolysis induced by the bacterial toxin, HlyA. These findings potentially have clinical perspectives as P2 antagonists may ameliorate symptoms during sepsis with hemolytic bacteria.
机译：大肠杆菌是正常肠道菌群中主要的兼性细菌。但是，大肠杆菌也是造成大多数严重肠外感染的原因。在兼性和侵入性大肠杆菌菌株之间存在明显的血清型差异。侵袭性菌株经常产生毒力因子，例如α-溶血素（HlyA），通过在红细胞膜上形成孔而引起溶血。本研究表明，这种孔形成触发嘌呤能受体激活，以介导完全的溶血作用。非选择性ATP受体（P2）拮抗剂（PPADS，苏拉明）和ATP清除剂（apyrase，己糖激酶）的浓度依赖性地抑制HlyA诱导的马，鼠和人红细胞的裂解。对更具选择性的P2拮抗剂的反应模式表明，P2X_1和P2X_7受体均参与了HlyA诱导的所有三个物种的溶血。此外，我们的研究结果还提出了孔蛋白pannexin1在HlyA诱导的溶血中的作用，因为该通道的非选择性抑制剂显着降低了这三种物种的溶血作用。总之，P2X受体的激活以及可能的Pannexins会增加细菌毒素HlyA诱导的溶血作用。这些发现可能具有临床前景，因为P2拮抗剂可改善溶血细菌败血症时的症状。

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