Literature DB >> 24629894

Morphine increases hippocampal viral load and suppresses frontal lobe CCL5 expression in the LP-BM5 AIDS model.

Virginia D McLane1, Ling Cao2, Colin L Willis2.   

Abstract

Chronic opiate abuse accelerates the development of cognitive deficits in human immunodeficiency virus (HIV)-1 patients. To investigate morphine's effects on viral infection of the central nervous system, we applied chronic morphine treatment to the LP-BM5 murine acquired immunodeficiency syndrome (MAIDS) model. LP-BM5 infection induces proinflammatory cytokine/chemokine production, correlating to increased blood-brain barrier permeability. Morphine treatment significantly increased LP-BM5 viral load in the hippocampus, but not in the frontal lobe. Morphine reduced the chemokine CCL5 to non-infected levels in the frontal lobe, but not in the hippocampus. These data indicate a region-specific mechanism for morphine's effects on virally-induced neurocognitive deficits.
Copyright © 2014 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Blood–brain barrier; Claudin-5; Cytokines; HIV encephalitis; Neuroinflammation; Opiate abuse

Mesh:

Substances:

Year:  2014        PMID: 24629894      PMCID: PMC4026271          DOI: 10.1016/j.jneuroim.2014.02.010

Source DB:  PubMed          Journal:  J Neuroimmunol        ISSN: 0165-5728            Impact factor:   3.478


  49 in total

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2.  Long-term morphine delivery via slow release morphine pellets or osmotic pumps: Plasma concentration, analgesia, and naloxone-precipitated withdrawal.

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