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. 1992;1(3):191–196. doi: 10.1155/S0962935192000292

Tumour necrosis factor-α mediates blood—brain barrier damage in HIV-1 infection of the central nervous system

M K Sharief 1,, M Ciardi 1, E J Thompson 1, F Sorice 2, F Rossi 2, V Vullo 2, A Cirelli 3
PMCID: PMC2365337  PMID: 18475460

Abstract

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-α (TNF-α) and interleukin-1β (IL-1β) in mediating disruption of the blood–brain barrier. Levels of TNF-α were more elevated in cerebrospinal fluid (CSF) than in serum of HIV-1 infected patients and were mainly detected in those patients who had neurologic involvement. Intrathecal TNF-α levels correlated with signs of blood–brain barrier damage, manifested by high CSF to serum albumin quotient, and with the degree of barrier impairment. In contrast, intrathecal IL-1β levels did not correlate with blood-brain barrier damage in HIV-1 infected patients. TNF-α seems to be related to active neural inflammation and to blood–brain barrier damage. The proinflammatory effects of TNF-α in the nervous system are dissociated from those of IL-1β.

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Selected References

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