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Analysis of Simian Immunodeficiency Virus-specific CD8+ T-cells in Rhesus Macaques by Peptide-MHC-I Tetramer Staining
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Chronic Binge Alcohol-Associated Differential Brain Region Modulation of Growth Factor Signaling Pathways and

John K Maxi1, Don Mercante2,3, Brittany Foret1

  • 1Department of Physiology, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, USA.

Alcohol and Alcoholism (Oxford, Oxfordshire)
|July 20, 2019
PubMed
Abstract

Insights

Chronic binge alcohol and SIV infection impact brain regions differently. Growth factor signaling in the prefrontal cortex and inflammation in the caudate and hippocampus may drive neuroinflammation and cognitive deficits.

Area of Science:

  • Neuroscience
  • Immunology
  • Toxicology

Background:

  • Chronic binge alcohol (CBA) administration and simian immunodeficiency virus (SIV) infection in macaques are associated with cognitive deficits.
  • Previous microarray analysis suggests altered immune response and neurogenesis as underlying mechanisms.

Purpose of the Study:

  • To investigate the differential brain region associations between neuroinflammation markers, growth factor signaling, and microtubule-associated protein 2 (MAP2) expression.
  • To explore the role of brain-derived neurotrophic factor (BDNF) in the prefrontal cortex.

Main Methods:

  • Adult male rhesus macaques received CBA or sucrose (control) for 3 months before SIV infection, continuing until end-stage disease.
  • Expression of inflammatory cytokines, growth factors, and viral loads were measured in the prefrontal cortex (PFC), caudate (CD), and hippocampus (HP).
  • BDNF expression and downstream signaling were analyzed in the PFC.

Main Results:

  • Reduced MAP2 expression was observed in the PFC of CBA/SIV macaques.
  • BDNF expression strongly correlated with MAP2 in the PFC.
  • In the caudate, MAP2 positively associated with BDNF, survival time, and viral load, and negatively with CBA.
  • In the hippocampus, MAP2 positively associated with inflammatory cytokines and negatively with viral load and CBA.

Conclusions:

  • CBA differentially impacts growth factor and inflammatory cytokine expression and viral load across brain regions.
  • Suppressed growth factor signaling in the PFC may be a key neuropathological mechanism.
  • Inflammatory processes appear more significant in the caudate and hippocampus.

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