Utter Christopher, Serrano Adelfa E, Glod John W, Leibowitz Michael J
Evolution Medical Communications, One Blue Hill Plaza, Pearl River, NY.
Department of Microbiology and Medical Zoology, University of Puerto Rico School of Medicine, San Juan, Puerto Rico.
Yale J Biol Med. 2017 Jun 23;90(2):183-193. eCollection 2017 Jun.
Endothelial abnormalities play a critical role in the pathogenesis of malaria caused by the human pathogen, . In serious infections and especially in cerebral malaria, red blood cells infected with the parasite are sequestered in small venules in various organs, resulting in endothelial activation and vascular occlusion, which are believed to be largely responsible for the morbidity and mortality caused by this infection, especially in children. We demonstrate that after incubation with infected red blood cells (iRBCs), cultured human umbilical vein endothelial cells (HUVECs) contain parasite protein, genomic DNA, and RNA, as well as intracellular vacuoles with apparent parasite-derived material, but not engulfed or adherent iRBCs. The association of this material with the HUVECs is observed over 96 hours after removal of iRBCs. This phenomenon may occur in endothelial cells by the process of trogocytosis, in which transfer of material between cells depends on direct cell contact. This process may contribute to the endothelial activation and disruption involved in the pathogenesis of cerebral malaria.
内皮细胞异常在由人类病原体引起的疟疾发病机制中起关键作用。在严重感染尤其是脑型疟疾中，感染寄生虫的红细胞会滞留在各个器官的小静脉中，导致内皮细胞活化和血管阻塞，据信这在很大程度上是这种感染所致发病和死亡的原因，尤其是在儿童中。我们证明，与感染的红细胞（iRBCs）孵育后，培养的人脐静脉内皮细胞（HUVECs）含有寄生虫蛋白、基因组DNA和RNA，以及带有明显寄生虫来源物质的细胞内空泡，但不含被吞噬或黏附的iRBCs。在去除iRBCs后96小时内均观察到这种物质与HUVECs的关联。这种现象可能在内皮细胞中通过胞饮作用发生，即细胞间物质转移依赖于直接的细胞接触。这一过程可能导致脑型疟疾发病机制中涉及的内皮细胞活化和破坏。
