Free circulating ICAM-1 in serum and cerebrospinal fluid of HIV-1 infected patients correlate with TNF-α and blood-brain barrier damage

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-α (TNF-α) mediates active neural inflammation and blood-brain barri...

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Main Authors: M. K. Sharief (Author), M. Ciardi (Author), M. A. Noori (Author), E. J. Thompson (Author), A. Salotti (Author), F. Sorice (Author), F. Rossi (Author), A. Cirelli (Author)
Format: Book
Published: Hindawi Limited, 1992-01-01T00:00:00Z.
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Summary: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-α (TNF-α) mediates active neural inflammation and blood-brain barrier damage in HIV-1 infection. Stimulation of endothelial cells by TNF-α 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-α 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.
Item Description:0962-9351
1466-1861
10.1155/S0962935192000486