| Autor: |
Utter C; Evolution Medical Communications, One Blue Hill Plaza, Pearl River, NY., Serrano AE; Department of Microbiology and Medical Zoology, University of Puerto Rico School of Medicine, San Juan, Puerto Rico., Glod JW; Center for Cancer Research, National Cancer Institute, Bethesda, MD., Leibowitz MJ; Department of Medical Microbiology & Immunology, University of California-Davis, Davis, CA. |
| Jazyk: |
angličtina |
| Zdroj: |
The Yale journal of biology and medicine [Yale J Biol Med] 2017 Jun 23; Vol. 90 (2), pp. 183-193. Date of Electronic Publication: 2017 Jun 23 (Print Publication: 2017). |
| Abstrakt: |
Endothelial abnormalities play a critical role in the pathogenesis of malaria caused by the human pathogen, Plasmodium falciparum . 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 in vivo 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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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