The internalization mechanism of Ureaplasma parvum in HeLa cells.

微小脲原体（U. parvum）是早产的原因，并定殖于人类泌尿生殖道。为了阐明U. paravum，U.将parvum用HeLa细胞攻击。联合感染后48 h内，HeLa细胞核周区有细小病毒聚集。美国的国际化。小孢子进入HeLa细胞被网格蛋白依赖性内吞抑制剂盐酸氯丙嗪（CPZ）和siRNA抑制。这些实验表明，U。parvum通过网格蛋白介导的内吞作用内化到HeLa细胞中。联合parvum与早到晚的内体标记共定位。在美国，观察到ROS的产生增加。小孢子虫感染细胞，导致线粒体嵴的结构变化和线粒体肿胀。我们的研究结果提出了CPZ可能在U.细小病毒感染

Ureaplasma parvum (U. parvum) is a causative of preterm delivery and colonizes human urogenital tract. In order to clarify the intracellular viability of U. paravum in the host cells, U. parvum was challenged to HeLa cells. U. parvum accumulated in the perinuclear region of the HeLa cells within 48 h after infection. Internalization of U. parvum into the HeLa cells was suppressed both by the clathrin-dependent endocytosis inhibitor chlorpromazine hydrochloride (CPZ) and the siRNA. These experiments indicated that U. parvum was internalized into HeLa cells via clathrin-mediated endocytosis. U. parvum were colocalized with early to late endosome markers. The increased production of ROS was observed in the U. parvum infected cells, which lead to structural changes in the mitochondrial cristae and swelling of mitochondria. Our findings raise the possibility that CPZ may have a potential role in the phylaxis of U. parvum infections.