Department of Neurochemistry Institute of Neurology The National Hospital for Neurology and Neurosurgery Queen Square London WC1N 3BG UK.
Mediators Inflamm. 1992;1(5):323-8. doi: 10.1155/S0962935192000486.
The mechanism for the initiation of blood-brain barrier damage and intrathecal inflammation in patients infected with the human immunodeficiency virus (HIV) is poorly understood. We have recently reported that tumour necrosis factor-alpha (TNF-alpha) mediates active neural inflammation and blood-brain barrier damage in HIV-1 infection. Stimulation of endothelial cells by TNF-alpha induces the expression of intercellular adhesion molecule-1 (ICAM-1), which is an important early marker of immune activation and response. We report herein for the first time the detection of high levels of free circulating ICAM-1 in serum and cerebrospinal fluid of patients with HIV-1 infection. Free circulating ICAM-1 in these patients correlated with TNF-alpha concentrations and with the degree of blood-brain barrier damage and were detected predominantly in patients with neurologic involvement. These findings have important implications for the understanding and investigation of the intrathecal inflammatory response in HIV-1 infection.
目前,人们对于感染人类免疫缺陷病毒(HIV)的患者血脑屏障损伤和鞘内炎症的发生机制知之甚少。我们最近的研究表明,肿瘤坏死因子-α(TNF-α)介导了 HIV-1 感染时的主动神经炎症和血脑屏障损伤。TNF-α刺激内皮细胞可诱导细胞间黏附分子-1(ICAM-1)的表达,ICAM-1 是免疫激活和应答的一个重要早期标志物。本研究首次报道,HIV-1 感染患者的血清和脑脊液中可检测到高水平的游离循环 ICAM-1。这些患者的游离循环 ICAM-1 与 TNF-α浓度以及血脑屏障损伤的程度相关,并且主要在伴有神经损伤的患者中检测到。这些发现对于理解和研究 HIV-1 感染时的鞘内炎症反应具有重要意义。