Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system: an evaluation of cytokines in cerebrospinal fluid
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2019, Brain ResearchCitation Excerpt :Many cytokines that promote inflammation, such as IL-1β, IL-6, IL-10, IL-12, IL-18 and TNF-α, are important inflammatory regulators associated with HIV infection (Saylor, 2016; Kraft-Terry, 2009; Burdo et al., 2013; Anthony and Bell, 2008; Brabers and Nottet, 2006). In particular, IL-6 and IL-1β are play an important role in HIV neuropathogenesis through immune mobilization, the activation of inflammatory cascades, and by increasing BBB permeability (Brabers and Nottet, 2006; Benveniste, 1994; Gallo, 1989). In the pre-cART era, elevated CSF IL-6 and IL-1β were often reported in individuals with HIV-dementia (Perrella, 1992; Eugenin, 2006), but have not been linked to cognitive impairment in the cART era (Yuan, 2013).
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2012, Neurochemistry InternationalCitation Excerpt :HIV associated neurocognitive disorder (HAND) is developed as a consequence of HIV infection in the central nervous system (CNS) occurring in about 50% of the HIV patients and is characterized by depression, behavioral and motor dysfunctions (Antinori et al., 2007; Ellis et al., 2007; McArthur and Brew, 2010). HIV infection in brain is associated with the release of several neurotoxic factors, generation of reactive oxygen species (ROS) (Ronaldson and Bendayan, 2008), stimulation of proinflammatory responses (Cysique et al., 2004; Gallo et al., 1989) eventually leading to cell death. The viral products implicated in the neurotoxicity of the HIV-1 infection include gp120, Tat, Nef, Vpr, Rev (Ellis et al., 2007; Nath and Geiger, 1998).
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2012, Frontiers in NeuroendocrinologyCitation Excerpt :IL-1β is very tightly regulated during the course of the immune response within the normal brain. Patients with AIDS-related dementia, cancer, chronic inflammatory diseases (e.g., Alzheimer’s), or autoimmune diseases often exhibit exaggerated levels of IL-1β co-occurring with cognitive impairment (Gallo et al., 1989; Griffin et al., 1989; Meyers, 2000). Exogenously applied IL-1β inhibits LTP within hippocampal slices (Cunningham et al., 1996; Katsuki et al., 1990), and similarly, a systemic injection of a high dose of LPS inhibits LTP of the hippocampal perforant pathway in vivo (Vereker et al., 2000).
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