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Central Nervous System Inflammation: Astroglia and Ethanol

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Encyclopedia of Neuroscience
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Synonyms

Alcohol; Astrocytes: Neuroinflammation

Definition

Long-term chronic and acute, binge-type alcohol (ethanol) consumption disrupts cognitive function and causes structural brain damage. The adverse effects of ethanol are typically realized when blood ethanol levels reach 20–50 mM; however, blood ethanol concentrations have been reported to exceed 200 mM. Among the cells profoundly affected by ethanol are the astroglia. Astroglia are the most prevalent cell type in the human central nervous system (CNS) and perform important roles both in normal tissue homeostasis and response to injury and infection. Physiological functions of astroglia include neurotrophic factor production, regulation of neuronal development and function, neurotransmitter metabolism and extracellular regulation of pH and K+concentration and they comprise a critical component of the blood-brain barrier (BBB). Important astroglial derived inflammatory mediators include cytokines, chemokines, inducible...

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References

  1. Molle I, Thulstrup AM, Svendsen N, Schonheyder HC, Sorensen HT (2000) Risk and case fatality rate of meningitis in patients with liver cirrhosis. Scand J Infect Dis 32:407–410

    Article  CAS  PubMed  Google Scholar 

  2. Pfefferbaum A, Rosenbloom M, Sullivan EV (2002) Alcoholism and AIDS: magnetic resonance imaging approaches for detecting interactive neuropathology. Alcohol Clin Exp Res 26:1031–1046

    Article  PubMed  Google Scholar 

  3. Flora G, Pu H, Lee YW, Ravikumar R, Nath A, Hennig B, Toborek M (2005) Proinflammatory synergism of ethanol and HIV-1 Tat protein in brain tissue. Exp Neurol 191:2–12

    Article  CAS  PubMed  Google Scholar 

  4. Davis RL, Syapin PJ (2004) Ethanol increases nuclear factor-κ B activity in human astroglial cells. Neurosci Lett 371:128–132

    Article  CAS  PubMed  Google Scholar 

  5. Guizzetti M, Bordi F, Dieguez-Acuna FJ, Vitalone A, Madia F, Woods JS, Costa LG (2003) Nuclear factor κB activation by muscarinic receptors in astroglial cells: effect of ethanol. Neuroscience 120:941–950

    Article  CAS  PubMed  Google Scholar 

  6. Davis RL, Syapin PJ (2005) Interactions of alcohol and nitric-oxide synthase in the brain. Brain Res Rev 49:494–504

    Article  CAS  PubMed  Google Scholar 

  7. Luo J, Lindstrom CL, Donahue A, Miller MW (2001) Differential effects of ethanol on the expression of cyclo-oxygenase in cultured cortical astrocytes and neurons. J Neurochem 76:1354–1363

    Article  CAS  PubMed  Google Scholar 

  8. Blanco AM, Valles SL, Pascual M, Guerri C (2005) Involvement of TLR4/type I IL-1 receptor signaling in the induction of inflammatory mediators and cell death induced by ethanol in cultured astrocytes. J Immunol 175:6893–6899

    Article  CAS  PubMed  Google Scholar 

  9. DeVito WJ, Stone S, Mori K, Shamgochian M (2000) Ethanol inhibits prolactin- and tumor necrosis factor-α-, but not γ interferon-induced expression of intercellular adhesion molecule-1 in human astrocytoma cells. J Cell Biochem 77:455–464

    Article  CAS  PubMed  Google Scholar 

  10. Davis RL, Syapin PJ (2004) Chronic ethanol inhibits CXC chemokine ligand 10 production in human A172 astroglia and astroglial-mediated leukocyte chemotaxis. Neurosci Lett 362:220–225

    Article  CAS  PubMed  Google Scholar 

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Davis, R.L. (2009). Central Nervous System Inflammation: Astroglia and Ethanol. In: Binder, M.D., Hirokawa, N., Windhorst, U. (eds) Encyclopedia of Neuroscience. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-29678-2_898

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