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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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Detalles Bibliográficos
Autores principales: Sharief, M. K., Ciardi, M., Noori, M. A., Thompson, E. J., Salotti, A., Sorice, F., Rossi, F., Cirelli, A.
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 1992
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365354/
https://www.ncbi.nlm.nih.gov/pubmed/18475479
http://dx.doi.org/10.1155/S0962935192000486
Descripción
Sumario: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.