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Production of Interleukin-8 by Human Neutrophils Stimulated with Trichomonas vaginalis

机译：人中性粒细胞刺激阴道滴虫产生白细胞介素8。

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Neutrophils are the predominant inflammatory cells found in the vaginal discharges of patients infected with Trichomonas vaginalis. Although chemoattractants, such as leukotriene B4 and interleukin-8 (IL-8), are found in the vaginal discharges of symptomatic trichomoniasis patients, little is known about the mechanism of how neutrophils accumulate or mediate initial inflammatory response after acute T. vaginalis infection. We examined IL-8 production in neutrophils activated by T. vaginalis and evaluated the factors involved in T. vaginalis adherence that might affect IL-8 production. When human neutrophils were stimulated with live trophozoites, T. vaginalis lysate, or T. vaginalis excretory-secretory products, the live trichomonads induced higher levels of IL-8 production than the lysate or products did. When live trichomonads were pretreated with various inhibitors of proteinase, microtubule, microfilament, or adhesin (which are all known to participate in the adherence of T. vaginalis to vaginal epithelial cells), IL-8 production significantly decreased compared with the untreated controls. Furthermore, an NF-κB inhibitor (pyrrolidine dithiocarbamate), a mitogen-activated protein (MAP) kinase (MEK) inhibitor (PD98059), and a p38 MAP kinase inhibitor (SB203580) significantly suppressed IL-8 synthesis in neutrophils. These results suggest that live T. vaginalis, particularly adherent trophozoites, can induce IL-8 production in neutrophils and that this action may be mediated through the NF-κB and MAP kinase signaling pathways. In other words, T. vaginalis-induced neutrophil recruitment may be mediated via the IL-8 expressed by neutrophils in response to activation by live T. vaginalis.
机译：中性粒细胞是感染阴道毛滴虫患者阴道分泌物的主要炎症细胞。虽然在症状性滴虫病患者的阴道分泌物中发现了白三烯B 4 和白细胞介素8（IL-8）等化学引诱剂，但对中性粒细胞如何累积或介导初始炎症的机制了解甚少急性 T后的反应。阴道感染。我们检查了由 T激活的嗜中性白细胞中IL-8的产生。阴道并评估了 T的相关因素。阴道粘附可能会影响IL-8的产生。用活滋养体刺激人类嗜中性粒细胞时， T。阴道裂解液或 T。阴道分泌物-分泌产物中，活滴虫诱导的IL-8生成水平高于溶解产物或产物。当用各种蛋白酶，微管，微丝或粘附素抑制剂（已知它们都参与 T。阴道杆菌对阴道上皮细胞的粘附）预处理活滴虫时，IL-8的产量显着降低与未处理的对照组相比。此外，NF-κB抑制剂（吡咯烷二硫代氨基甲酸酯），促分裂原活化蛋白（MAP）激酶（MEK）抑制剂（PD98059）和p38 MAP激酶抑制剂（SB203580）显着抑制中性粒细胞的IL-8合成。这些结果表明实况 T。阴道，特别是粘附的滋养体，可以诱导中性粒细胞产生IL-8，并且这种作用可能是通过NF-κB和MAP激酶信号通路来介导的。换句话说， T。阴道中性粒细胞募集可能通过中性粒细胞表达的IL-8介导，以响应活体T的激活。阴道。

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