三虫阴道粘附蛋白65 (TvAP65) 通过与宿主细胞蛋白相互作用来调节寄生虫的致病性
Zhenchao Zhang1, Xiaoxiao Song1, Yangyang Deng2
1Department of Pathogenic Biology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, Henan, 453003, PR China; Xinxiang Key Laboratory of Pathogenic Biology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, Henan, 453003, PR China.
Acta tropica
|August 3, 2023
概括
特里科莫纳斯阴道粘附蛋白65 (TvAP65) 对于宿主细胞入侵至关重要. 它与BNIP3的相互作用调解了寄生虫粘附和致病性,为三病治疗提供了潜在的药物标.
科学领域:
- 寄生虫学的寄生虫学
- 分子生物学分子生物学
- 传染性疾病 传染性疾病
背景情况:
- 阴道虫 (Trichomonas vaginalis) 是一个重要的性传播病原体.
- 宿主细胞粘附对于T. vaginalis寄生和致病性至关重要.
- 粘附蛋白65 (TvAP65) 与T. vaginalis粘附有关,但其确切作用尚不清楚.
研究的目的:
- 阐明TvAP65在T. vaginalis粘附和致病性中的作用.
- 识别与TvAP65.65相互作用的宿主细胞分子.
- 为了研究TvAP65与宿主细胞相互作用在三病中的功能意义.
主要方法:
- 通过小RNA干扰,降低了T. vaginalis.中的TvAP65表达.
- 用VK2/E6E7细胞培养来评估寄生虫粘附和宿主细胞反应.
- 动物挑战实验和被动免疫用于病原性评估.
- 酵母两杂交系统和共免疫沉以识别和确认蛋白质相互作用.
- 免疫光和局部化研究可视化蛋白质结合.
主要成果:
- 抑制TvAP65显著降低了T. vaginalis对宿主细胞的附着性,并减少了宿主细胞的损伤.
- 用抗TvAP65抗体或阻断TvAP65的被动免疫减少了寄生虫在体内的致病性.
- 发现tvAP65可以与VK2/E6E7细胞结合.
- 宿主蛋白BNIP3被确定为TvAP65.5的相互作用伙伴.
- 同时抑制TvAP65和BNIP3进一步降低了寄生虫粘附和宿主细胞增殖抑制.
结论:
- TvAP65通过与宿主细胞蛋白的相互作用来调解T. vaginalis粘附和致病性,包括BNIP3.
- 这种TvAP65-BNIP3相互作用是T. vaginalis发病的一个关键因素.
- 这项研究为开发针对T. vaginalis的新药向提供了基础,并提供了关于预防和治疗三虫病的见解.
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