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HIV-1 Tat-induced diarrhea evokes an enteric glia-dependent neuroinflammatory response in the central nervous system.

HIV-1 Tat-induced diarrhea evokes an enteric glia-dependent neuroinflammatory response in the central nervous system.
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Esposito G, Capoccia E, Gigli S, Pesce M, Bruzzese E, D'Alessandro A, Cirillo C, di Cerbo A, Cuomo R, Seguella L, Steardo L, Sarnelli G,


Esposito G, Capoccia E, Gigli S, Pesce M, Bruzzese E, D'Alessandro A, Cirillo C, di Cerbo A, Cuomo R, Seguella L, Steardo L, Sarnelli G, (click to view)

Esposito G, Capoccia E, Gigli S, Pesce M, Bruzzese E, D'Alessandro A, Cirillo C, di Cerbo A, Cuomo R, Seguella L, Steardo L, Sarnelli G,

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Scientific reports 2017 08 107(1) 7735 doi 10.1038/s41598-017-05245-9

Abstract

Despite the effectiveness of combined anti-retroviral therapy, human immunodeficiency virus (HIV) infected-patients frequently report diarrhea and neuropsychological deficits. It is claimed that the viral HIV-1 Trans activating factor (HIV-1 Tat) protein is responsible for both diarrhea and neurotoxic effects, but the underlying mechanisms are not known. We hypothesize that colonic application of HIV-1 Tat activates glial cells of the enteric nervous system (EGCs), leading to a neuroinflammatory response able to propagate to the central nervous system. We demonstrated that HIV-1 Tat-induced diarrhea was associated with a significant activation of glial cells within the colonic wall, the spinal cord and the frontal cortex, and caused a consistent impairment of the cognitive performances. The inhibition of glial cells activity by lidocaine, completely abolished the above-described effects. These observations point out the role of glial cells as putative effectors in HIV-1 Tat-associated gastrointestinal and neurological manifestations and key regulators of gut-brain signaling.

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