Division of Infectious Genetics, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Am J Trop Med Hyg. 2010 Jan;82(1):136-9. doi: 10.4269/ajtmh.2010.09-0203.
In cerebral malaria, the binding of parasitized erythrocytes to the cerebral endothelium and the consequent angiogenic dysregulation play a key role in pathogenesis. Because vascular endothelial growth factor (VEGF) is widely regarded as a potent stimulator of angiogenesis, edema, inflammation, and vascular remodeling, the plasma levels of VEGF and the soluble form of the VEGF receptor (sVEGFR)-1 and -2 in uncomplicated malaria patients and healthy adults were measured by enzyme-linked immunosorbent assay (ELISA) to examine their roles in malaria. The results showed that VEGF and sVEGFR-2 levels were significantly elevated in malaria patients compared with healthy adults. Moreover, it was confirmed that malarial parasite antigens induced VEGF secretion from the human mast cell lines HMC-1 or KU812 cell. This is the first report to suggest that the interaction of VEGF and sVEGFR-2 is involved in the host immune response to malarial infection and that malarial parasites induce VEGF secretion from human mast cells.
在脑型疟疾中，寄生红细胞与脑内皮细胞的结合以及由此导致的血管生成失调在发病机制中起着关键作用。因为血管内皮生长因子（VEGF）被广泛认为是血管生成、水肿、炎症和血管重塑的有效刺激物，所以通过酶联免疫吸附试验（ELISA）测量了无并发症疟疾患者和健康成年人血浆中的 VEGF 水平以及可溶性 VEGF 受体（sVEGFR）-1 和 -2 的水平，以研究它们在疟疾中的作用。结果表明，与健康成年人相比，疟疾患者的 VEGF 和 sVEGFR-2 水平显著升高。此外，已经证实疟原虫抗原可诱导人肥大细胞系 HMC-1 或 KU812 细胞分泌 VEGF。这是第一项表明 VEGF 和 sVEGFR-2 的相互作用参与宿主对疟原虫感染的免疫反应的报告，并且疟原虫可诱导人肥大细胞分泌 VEGF。
