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首页> 外文期刊>Infection and immunity >Distinct Susceptibilities of Corneal Pseudomonas aeruginosa Clinical Isolates to Neutrophil Extracellular Trap-Mediated Immunity
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Distinct Susceptibilities of Corneal Pseudomonas aeruginosa Clinical Isolates to Neutrophil Extracellular Trap-Mediated Immunity

机译：铜绿假单胞菌铜绿假单胞菌临床分离株对嗜中性粒细胞胞外诱集免疫的敏感性

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Ocular bacterial keratitis, often associated with Pseudomonas aeruginosa bacterial infection, commonly occurs in contact lens wearers and may lead to vision impairment. In this study, we analyzed the contribution of neutrophil extracellular traps (NETs) to the mediation of protection during ocular keratitis. Both invasive and cytotoxic P. aeruginosa clinical isolates induced NET release by neutrophils. NETs carried the characteristic histone proteins, elastase, lysozyme, myeloperoxidase, and metabolic enzymes. While the invasive P. aeruginosa strains PAO1 (serogroup O5) and 6294 (serogroup O6) were trapped by NETs, the cytotoxic P. aeruginosa strains 6077, 6206 (serogroup O11), and PA14 (serogroup 010) were less sensitive to NET capture. The mechanism of escape by the cytotoxic strains from adhesion to NETs involved the shedding of outer membrane vesicles (OMVs) that outcompeted the cytotoxic P. aeruginosa strains for NET binding. When ocular infection was caused by an invasive strain in vivo, NETs were released at the ocular surface to capture bacteria, limiting their spread. Treatment with MNase I had a dose-dependent effect, with low doses of MNase speeding up bacterial clearance and high doses of MNase having toxic consequences. Cumulatively, our data suggest that NET-mediated immunity is a two-step process. Initially, pathogens attach to NET fragments; subsequently, upon nuclease activity, active serine proteases, which proteolytically degrade NET-associated proteins and promote DNase activity, are released. Therefore, a balance between NET production and NET degradation is needed to achieve maximal NET immunity.
机译：眼细菌性角膜炎通常与铜绿假单胞菌细菌感染有关，通常发生在隐形眼镜配戴者中，并可能导致视力障碍。在这项研究中，我们分析了中性粒细胞胞外诱捕器（NETs）对眼角膜炎期间保护介导的作用。侵入性和细胞毒性铜绿假单胞菌临床分离株均诱导嗜中性粒细胞释放NET。 NETs带有特征性的组蛋白，弹性蛋白酶，溶菌酶，髓过氧化物酶和代谢酶。 NET捕获了侵入性铜绿假单胞菌菌株PAO1（O5血清型）和6294（O6血清型），而细胞毒性铜绿假单胞菌6077、6206（O11血清型）和PA14（010血清型）对NET捕获的敏感性较低。细胞毒性毒株从粘附到NET逃逸的机制涉及外膜囊泡（OMV）的脱落，后者比铜绿假单胞菌菌株对NET的竞争要强。当眼内感染是由体内的侵入性菌株引起时，NETs在眼表面释放以捕获细菌，从而限制了细菌的传播。 MNase I的治疗具有剂量依赖性，低剂量的MNase可以加速细菌清除，而高剂量的MNase则具有毒性后果。累积地，我们的数据表明，NET介导的免疫是一个两步过程。最初，病原体会附着在NET片段上。随后，以核酸酶活性为基础，释放了蛋白水解降解NET相关蛋白并促进DNase活性的活性丝氨酸蛋白酶。因此，需要在NET产生和NET降级之间取得平衡，以实现最大的NET抗扰性。

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