Free circulating ICAM-1 in serum and cerebrospinal fluid of HIV-1 infected patients correlate with TNF-α and blood-brain barrier damage
نویسندگان
چکیده
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.
منابع مشابه
Tumour necrosis factor-α mediates blood—brain barrier damage in HIV-1 infection of the central nervous system
The pathogenesis of brain inflammation and damage by human immunodeficiency virus (HIV) infection is unclear. Because blood-brain barrier damage and impaired cerebral perfusion are common features of HIV-1 infection, we evaluated the role of tumour necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in mediating disruption of the blood-brain barrier. Levels of TNF-alpha were more...
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عنوان ژورنال:
- Mediators of Inflammation
دوره 1 شماره
صفحات -
تاریخ انتشار 1992