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首页> 外文期刊>Journal of Reproductive Immunology >Polymicrobial stimulation of human fetal membranes induce neutrophil activation and neutrophil extracellular trap release
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Polymicrobial stimulation of human fetal membranes induce neutrophil activation and neutrophil extracellular trap release

机译：人胎膜的多发性刺激诱导中性粒细胞活化和中性粒细胞细胞外陷阱释放

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Preterm birth is a major contributor to neonatal mortality and morbidity. While the causes of preterm birth remain incompletely understood, infection is a major risk factor, and chorioamnionitis is commonly observed. Chorioamnionitis is characterized by inflammation and neutrophil infiltration of the fetal membranes (FM). We recently reported that human FMs which had been exposed to low levels of bacterial lipopolysaccharide (LPS) recruit neutrophils and activate them, increasing their secretion of pro-inflammatory cytokines, degranulation of myeloperoxidase (MPO), and release of neutrophil extracellular traps (NETs). Herein, we demonstrate that conditioned media (CM) from viral dsRNA (Poly(I:C))-stimulated FMs also increased neutrophil migration, and induced the secretion of inflammatory IL-8 and the release of NETs. Furthermore, CM from FMs stimulated by a combination of bacterial LPS and Poly(I:C) augmented neutrophil NET release, compared to CM from FMs stimulated with either Poly(I:C) or LPS alone. NETs induced by FMs exposed to Poly(I:C), with or without LPS, were released and degraded quicker than those induced by resting or LPS-stimulated FM-CM. These findings indicate that FMs exposed to viral dsRNA promote neutrophil recruitment, activation and NET formation, similar to FMs exposed to bacterial LPS alone. However, in response to FM polymicrobial stimulation the levels and kinetics of NET release are augmented. This work builds upon our understanding of how infections at the maternal-fetal interface may affect neutrophil function.
机译：早产是新生儿死亡率和发病率的主要原因。虽然早产的原因尚不完全清楚，但感染是一个主要的危险因素，绒毛膜羊膜炎是常见的。绒毛膜羊膜炎的特征是炎症和中性粒细胞浸润胎膜（FM）。我们最近报道，暴露于低水平细菌脂多糖（LPS）的人类FMs招募中性粒细胞并激活它们，增加其促炎细胞因子的分泌、髓过氧化物酶（MPO）脱颗粒和中性粒细胞胞外陷阱（NET）的释放。在此，我们证明了由病毒dsRNA（Poly（I:C））刺激的FMs产生的条件培养基（CM）也增加了中性粒细胞的迁移，并诱导炎性IL-8的分泌和net的释放。此外，细菌LPS和聚（I:C）联合刺激的FMs CM增加了中性粒细胞的净释放，而单用聚（I:C）或LPS刺激的FMs CM增加了中性粒细胞的净释放。与静息或LPS刺激的FM-CM相比，暴露于含或不含LPS的聚（I:C）的FMs诱导的NET释放和降解更快。这些发现表明，暴露于病毒性dsRNA的FMs促进中性粒细胞的募集、激活和网络形成，与单独暴露于细菌LPS的FMs相似。然而，在FM多微生物刺激下，净释放的水平和动力学增加。这项工作建立在我们对母胎界面感染如何影响中性粒细胞功能的理解之上。

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