Abstract：
Trichomonas vaginalis causes trichomoniasis, the most common non-viral sexually transmitted disease worldwide. As an extracellular parasite, adhesion to host cells is essential for the development of infection. During attachment, the parasite changes its tear ovoid shape to a flat ameboid form, expanding the contact surface and migrating through tissues. Here, we have identified a novel structure formed at the posterior pole of adherent parasite strains, resembling the previously described uropod, which appears to play a pivotal role as an anchor during the attachment process. Moreover, our research demonstrates that the overexpression of the tetraspanin T. vaginalis TSP5 protein (TvTSP5), which is localized on the cell surface of the parasite, notably enhances the formation of this posterior anchor structure in adherent strains. Finally, we demonstrate that parasites that overexpress TvTSP5 possess an increased ability to adhere to host cells, enhanced aggregation and reduced migration on agar plates. Overall, these findings unveil novel proteins and structures involved in the intricate mechanisms of T. vaginalis interactions with host cells.
摘要：
阴道毛滴虫引起毛滴虫病,全球最常见的非病毒性性传播疾病。作为一种细胞外寄生虫，与宿主细胞的粘附对于感染的发展至关重要。在附件期间，寄生虫将其泪液卵形变成扁平的阿米波形态，扩大接触面并通过组织迁移。这里,我们已经确定了在粘附寄生虫菌株的后极形成的新结构，类似于先前描述的尾足类，在依恋过程中，它似乎作为锚点起着举足轻重的作用。此外，我们的研究表明，四跨膜蛋白TSP5蛋白（TvTSP5）的过表达，位于寄生虫的细胞表面，显着增强了粘附应变中这种后锚结构的形成。最后,我们证明过表达TvTSP5的寄生虫具有增加的寄生虫粘附宿主细胞的能力，增强寄生虫聚集和减少在琼脂平板上的迁移。总的来说,这些发现揭示了与阴道毛滴虫与宿主细胞相互作用的复杂机制有关的新型蛋白质和结构。
