van der Flier M, Coenjaerts F E, Mwinzi P N, Rijkers E, Ruyken M, Scharringa J, Kimpen J L L, Hoepelman A I M, Geelen S P M
Wilhelmina Children's Hospital, University Medical Center, Room KE 04.1331, P.O. Box 85090, 3508 AB Utrecht, The Netherlands.
J Neuroimmunol. 2005 Mar;160(1-2):170-7. doi: 10.1016/j.jneuroim.2004.11.013.
To determine the contribution of vascular endothelial growth factor (VEGF) to cerebral edema formation in bacterial meningitis, we used a VEGF neutralizing antibody to block VEGF in rabbits, following induction of meningitis by intracisternal inoculation with 10(9) heat-killed pneumococci. At 8 h, cerebrospinal fluid (CSF) VEGF was significantly elevated in infected untreated animals, and correlated with CSF white blood cell (WBC) count (r=0.56, P=0.004), and brain water content (r=0.42, P=0.04). Blocking of VEGF did not attenuate brain edema, blood-brain barrier disruption, or CSF pleocytosis. The functional role of VEGF in the pathophysiology of BM remains elusive.
为了确定血管内皮生长因子（VEGF）在细菌性脑膜炎脑水肿形成中的作用，我们通过脑池内接种10⁹ 热灭活肺炎球菌诱导家兔脑膜炎后，使用VEGF中和抗体来阻断VEGF。在8小时时，感染未治疗动物的脑脊液（CSF）VEGF显著升高，且与脑脊液白细胞（WBC）计数相关（r = 0.56，P = 0.004），与脑含水量相关（r = 0.42，P = 0.04）。阻断VEGF并未减轻脑水肿、血脑屏障破坏或脑脊液细胞增多。VEGF在细菌性脑膜炎病理生理学中的功能作用仍不清楚。
