Proinflammatory Cytokine and Nitric Oxide Production by Human Macrophages Stimulated with Trichomonas vaginalis
Proinflammatory Cytokine and Nitric Oxide Production by Human Macrophages Stimulated with Trichomonas vaginalis
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DOI：
10.3347/kjp.2009.47.3.205
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发表时间：
2009-09-01
影响因子：
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通讯作者：
Ryu, Jae-Sook
中科院分区：
文献类型：
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作者：
Han, Ik-Hwan;Goo, Sung Young;Ryu, Jae-Sook
阴道毛滴虫通常会引起阴道炎，女性可能会引起宫颈炎，男性和女性可能会引起尿道炎。巨噬细胞是重要的免疫细胞，对T。迷走神经感染在这项研究中，我们研究了人类巨噬细胞是否参与T.流浪汉人单核细胞源性巨噬细胞（HMDM）与T.流浪汉活的、调理活的毛滴虫和T.迷走细胞裂解物增加HMDM引起的促炎细胞因子，如TNF-α、IL-1 β和IL-6。核因子（NF）-κ B B信号通路参与T.通过p65 NF-κ B的磷酸化和核转位证实了迷走神经损伤。此外，用活T.迷走神经刺激诱导HMDM中一氧化氮（NO）产生和诱导型NO合酶（iNOS）水平的表达显著增加。然而，滴虫诱导的NF-κ B活化和TNF-α的产生在巨噬细胞中被L-NMMA（NO合成酶抑制剂）抑制iNOS水平显著抑制。此外，用NF-κ B抑制剂（PDTC或Bay 11 -7082）预处理导致人巨噬细胞产生较少的TNF-α。这些结果表明T.迷走神经刺激人巨噬细胞产生促炎细胞因子，如IL-1、IL-6、TNF-α和NO。迷走神经损伤通过NO依赖性激活NF-κ B B诱导巨噬细胞产生TNF-α，可能与T.流浪汉
Trichomonas vaginalis commonly causes vaginitis and perhaps cervicitis in women and urethritis in men and women. Macrophages are important immune cells in response to T. vaginalis infection. In this study, we investigated whether human macrophages could be involved in inflammation induced by T. vaginalis. Human monocyte-derived macrophages ( HMDM) were co-cultured with T. vaginalis. Live, opsonized-live trichomonads, and T. vaginalis lysates increased proinflammatory cytokines, such as TNF-alpha, IL-1 beta, and IL-6 by HMDM. The involvement of nuclear factor (NF)-kappa B signaling pathway in cytokine production induced by T. vaginalis was confirmed by phosphorylation and nuclear translocation of p65 NF-kappa B. In addition, stimulation with live T. vaginalis induced marked augmentation of nitric oxide ( NO) production and expression of inducible NO synthase ( iNOS) levels in HMDM. However, trichomonad-induced NF-kappa B activation and TNF-alpha production in macrophages were significantly inhibited by inhibition of iNOS levels with L-NMMA ( NO synthase inhibitor). Moreover, pretreatment with NF-kappa B inhibitors ( PDTC or Bay11-7082) caused human macrophages to produce less TNF-alpha. These results suggest that T. vaginalis stimulates human macrophages to produce proinflammatory cytokines, such as IL-1, IL-6, and TNF-alpha, and NO. In particular, we showed that T. vaginalis induced TNF-alpha production in macrophages through NO-dependent activation of NF-kappa B, which might be closely involved in inflammation caused by T. vaginalis.