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      Microglia activation by SIV-infected macrophages: alterations in morphology and cytokine secretion

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          Abstract

          HIV infection in brain and the resultant encephalitis affects approximately one-third of individuals infected with HIV, regardless of treatment with antiretroviral drugs. Microglia are the resident phagocytic cell type in the brain, serving as a “first responder” to neuroinvasion by pathogens. The early events of the microglial response to productively-infected monocyte/macrophages entering the brain can best be investigated using in vitro techniques. We hypothesized that activation of microglia would be specific to the presence of SIV-infected macrophages as opposed to responses to macrophages in general. Purified microglia were grown and stimulated with control or SIV-infected macrophages. After 6 hours, aliquots of supernatant were analyzed for 23 cytokines using Millipore non-human primate-specific kit. In parallel experiments, morphologic changes and cytokine expression by individual microglia were examined by immunofluorescence. Surprisingly, the presence of macrophages was more important to the microglial response rather than whether the macrophages were infected with SIV. None of the cytokines examined was unique to co-incubation with SIV-infected macrophages compared with control macrophages, or their supernatants. Media from SIV-infected macrophages, however, did induce secretion of higher levels of IL-6 and IL-8 than the other treatments. As resident macrophages in the brain, microglia would be expected to have a strong response to infiltrating innate immune cells such as monocyte/macrophages. This response is triggered by incubation with macrophages, irrespective of whether or not they are infected with SIV, indicating a rapid, generalized immune response when infiltrating macrophages enter brain.

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          Author and article information

          Journal
          9508123
          20381
          J Neurovirol
          J. Neurovirol.
          Journal of Neurovirology
          1355-0284
          1538-2443
          27 April 2012
          26 April 2012
          June 2012
          01 June 2013
          : 18
          : 3
          : 213-221
          Affiliations
          [1 ]Tulane National Primate Research Center, Tulane University, New Orleans, LA
          [2 ]Tulane Program in Neuroscience, Tulane University, New Orleans, LA
          [3 ]Department of Microbiology & Immunology, Tulane University, New Orleans, LA
          [4 ]Department of Cell and Molecular Biology, Tulane University, New Orleans, LA
          Author notes
          [* ]Corresponding author: Division of Comparative Pathology, Tulane National Primate Research Center, Covington, LA 70433., ‘Phone: 985-871-6489, amaclean@ 123456tulane.edu
          Article
          PMC3361629 PMC3361629 3361629 nihpa373218
          10.1007/s13365-012-0100-7
          3361629
          22535448
          863f053e-f093-4e39-9f22-08e22130fdc0
          History
          Categories
          Article

          cytokine,neuropathogenesis,neuroinflammation,HIV,microglia,chemokine

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