Cerebrospinal fluid levels of chemokines in HIV infected patients with and without opportunistic infection of the central nervous system.

Authors:
Paulo Pereira Christo
Paulo Pereira Christo
Santa Casa de Belo Horizonte Hospital
Brazil
Renan Barros Domingues
Renan Barros Domingues
Federal University of Minas Gerais
Brazil
Dirceu Bartolomeu Greco
Dirceu Bartolomeu Greco
Federal University of Minas Gerais
Brazil
Jose Antonio Livramento
Jose Antonio Livramento
Eduardo de Menezes Hospital
Brazil
Antonio Lucio Teixeira
Antonio Lucio Teixeira
University Hospital
Brazil

J Neurol Sci 2009 Dec 25;287(1-2):79-83. Epub 2009 Sep 25.

Neurology Unit, University Hospital, Federal University of Minas Gerais, Belo Horizonte, Brazil.

Chemokines are chemoattractant cytokines involved in the immune response of a wide variety of diseases. There are few studies assessing their role in opportunistic infections in HIV-infected patients. In this study, we measured CC and CXC chemokines in cerebrospinal fluid (CSF) samples obtained from 40 HIV-infected patients with or without opportunistic infections of the central nervous system (CNS). CSF samples were also analyzed for quantification of total protein, cell count and HIV-1 RNA. HIV+ patients with cryptococcal meningitis had higher levels of CCL2, CCL3, CCL5, CXCL9 and CXCL10 when compared to patients without opportunistic neurological infections. Furthermore, HIV+ patients with associated cryptococcal meningitis had higher levels of CCL3, CXCL9 and CXCL10 when compared to HIV+ patients with associated toxoplasmic encephalitis. CCL3 and CXCL9 levels were positively correlated with CSF HIV-1 RNA levels, CSF protein concentration, and CSF cell count. CXCL10 level was correlated with the CSF viral load and the CSF cell count and CCL5 level was correlated with the CSF cell count. In conclusion, the profile of chemokines in CSF of HIV patients may differ according to the modality of the presented opportunistic infection and according to other biological markers, such as viral load in CSF. These differences are probably related to different patterns of neuroinflammatory responses displayed by patients with different opportunistic neurological infections.

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http://dx.doi.org/10.1016/j.jns.2009.09.002DOI Listing
December 2009
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