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The Journal of Neuroscience, March 9, 2005, 25(10):2530-2536; doi:10.1523/JNEUROSCI.3923-04.2005

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Cellular/Molecular
A Glial Endogenous Cannabinoid System Is Upregulated in the Brains of Macaques with Simian Immunodeficiency Virus-Induced Encephalitis

Cristina Benito,¹ Wong-Ki Kim,² Iván Chavarría,^1,3 Ceceila J. Hillard,⁴ Ken Mackie,⁵ Rosa M. Tolón,¹ Ken Williams,² and Julián Romero^1,3

¹Laboratorio de Apoyo a la Investigación, Fundación Hospital Alcorcón, 28922 Madrid, Spain, ²Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, ³Department of Biochemistry, Francisco de Vitoria University, Pozuelo de Alarcón, 28223 Madrid, Spain, ⁴Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, and ⁵Department of Anesthesiology, University of Washington, Seattle, Washington 98195

Recent evidence supports the notion that the endocannabinoid system may play a crucial role in neuroinflammation. We explored the changes that some elements of this system exhibit in a macaque model of encephalitis induced by simian immunodeficiency virus. Our results show that profound alterations in the distribution of specific components of the endocannabinoid system occur as a consequence of the viral infection of the brain. Specifically, expression of cannabinoid receptors of the CB₂ subtype was induced in the brains of infected animals, mainly in perivascular macrophages, microglial nodules, and T-lymphocytes, most likely of the CD8 subtype. In addition, the endogenous cannabinoid-degrading enzyme fatty acid amide hydrolase was overexpressed in perivascular astrocytes as well as in astrocytic processes reaching cellular infiltrates. Finally, the pattern of CB₁ receptor expression was not modified in the brains of infected animals compared with that in control animals. These results resemble previous data obtained in Alzheimer's disease human tissue samples and suggest that the endocannabinoid system may participate in the development of human immunodeficiency virus-induced encephalitis, because activation of CB₂ receptors expressed by immune cells is likely to reduce their antiviral response and thus could favor the CNS entry of infected monocytes.

Key words: neuroinflammation; viral encephalitis; gliosis; endocannabinoids; immunohistochemistry; macaques

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Received Sep 22, 2004; revised January 5, 2005; accepted January 13, 2005.

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				C. Benito, J. P. Romero, R. M. Tolon, D. Clemente, F. Docagne, C. J. Hillard, C. Guaza, and J. Romero Cannabinoid CB1 and CB2 Receptors and Fatty Acid Amide Hydrolase Are Specific Markers of Plaque Cell Subtypes in Human Multiple Sclerosis J. Neurosci., February 28, 2007; 27(9): 2396 - 2402. [Abstract] [Full Text] [PDF]

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