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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
Author(s) -
M. K. Sharief,
Maria Rosa Ciardi,
M. A. Noori,
E J Thompson,
A Salotti,
F Sorice,
Federica Rossi,
A Cirelli
Publication year - 1992
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1155/s0962935192000486
Subject(s) - cerebrospinal fluid , icam 1 , blood–brain barrier , tumor necrosis factor alpha , inflammation , immunology , medicine , intercellular adhesion molecule 1 , immune system , cell adhesion molecule , pathology , central nervous system
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.

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