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Trichomonas vaginalis-secreted cysteinyl leukotrienes promote migration, degranulation and MCP-1 production in mast cells.
Parasite Immunology ( IF 2.2 ) Pub Date : 2020-09-03 , DOI: 10.1111/pim.12789
Young Ah Lee 1 , Young Hee Nam 1 , Arim Min 1 , Myeong Heon Shin 1
Affiliation  

Trichomonas vaginalis, a flagellated extracellular protozoan parasite that infects the human genitourinary tract, is usually transmitted by sexual contact. Our previous study showed that the leukotriene B4 (LTB4), a T vaginalis‐secreted lipid mediator, induces interleukin (IL)‐8 production and promotes mast cell degranulation and migration via BLT1 in human. In this study, we investigated whether T vaginalis produces another leukotrienes and whether it causes increased MCP‐1 production, mast cell migration and degranulation by activating mast cells. We found that cysteinyl leukotrienes (CysLTs) were contained in T vaginalis‐derived secretory product (TvSP) by ELISA. The TvSP‐stimulated human mast cell line (HMC‐1) exhibited significantly increased monocyte chemoattractant protein‐1 (MCP‐1) secretion compared to the unstimulated cells. Inhibition of NOX2 activation of cells by treatment of NOX inhibitor or NOX2 siRNA reduced TvSP‐stimulated MCP‐1 production in HMC‐1 cells. It was also confirmed that the receptor for CysLTs is expressed in mast cells. The CysLT receptor (CysLTR) antagonist inhibited TvSP‐stimulated MCP‐1 production of mast cells, as well as ROS production, migration and degranulation of mast cells, and reduced phospho‐NF‐kB expression. These results suggest that T vaginalis‐secreted CysLTs promote migration, degranulation and MCP‐1 production in human mast cells through CysLT receptor‐mediated NOX2 activation.

中文翻译:

阴道毛滴虫分泌的半胱氨酰白三烯促进肥大细胞中的迁移,脱粒和MCP-1产生。

阴道毛滴虫(一种感染了人类泌尿生殖道的鞭毛细胞外原生动物寄生虫)通常通过性接触传播。我们以前的研究表明,白三烯B 4(LTB 4)是T阴道分泌的脂质介体,可诱导白介素(IL)-8的产生,并促进肥大细胞脱粒和通过人BLT1迁移。在这项研究中,我们调查了T阴道杆菌是否产生另一种白三烯,以及是否通过激活肥大细胞引起MCP-1产量增加,肥大细胞迁移和脱粒。我们发现半胱氨酸白三烯(CysLTs)包含在T阴道ELISA衍生的分泌产物(TvSP)。与未刺激的细胞相比,TvSP刺激的人类肥大细胞系(HMC-1)分泌的单核细胞趋化蛋白-1(MCP-1)分泌显着增加。通过处理NOX抑制剂或NOX2 siRNA抑制细胞的NOX2活化,可降低TvSP刺激的HMC-1细胞中MCP-1的产生。还证实了CysLTs的受体在肥大细胞中表达。CysLT受体(CysLTR)拮抗剂抑制TvSP刺激的肥大细胞MCP-1产生,肥大细胞的ROS产生,迁移和脱粒以及磷酸化NF-kB的表达降低。这些结果表明,T阴道分泌的CysLTs通过CysLT受体介导的NOX2活化促进了人类肥大细胞的迁移,脱粒和MCP-1产生。
更新日期:2020-11-12
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