This article represents the proceedings of a symposium at the 2005 RSA Meeting in Santa Barbara, CA, organized and chaired by Fulton T. Crews. The presentations and presenters were: (1) Cytokines and Alcohol, Fulton Crews; (2) Alteration of the Cytokine Profile of Circulating Human Monocytes by Alcohol, Gyongyi Szabo; (3) Impaired Cytokine Regulation Renders the Alcoholic Lung Susceptible to Injury from Both Aberrant Immune Activation and Immune Suppression, David Guidot; (4) Cytokines And Alcoholic Liver Disease.
Cytokines and Alcohol
Version of Record online: 29 MAR 2006
Alcoholism: Clinical and Experimental Research
Volume 30, Issue 4, pages 720–730, April 2006
How to Cite
Crews, F. T., Bechara, R., Brown, L. A., Guidot, D. M., Mandrekar, P., Oak, S., Qin, L., Szabo, G., Wheeler, M. and Zou, J. (2006), Cytokines and Alcohol. Alcoholism: Clinical and Experimental Research, 30: 720–730. doi: 10.1111/j.1530-0277.2006.00084.x
- Issue online: 29 MAR 2006
- Version of Record online: 29 MAR 2006
- Received for publication September 28, 2005; accepted December 3, 2005.
Cytokines are multifunctional proteins that play a critical role in cellular communication and activation. Cytokines have been classified as being proinflammatory (T helper 1, Th1) or anti-inflammatory (T helper 2, Th2) depending on their effects on the immune system. However, cytokines impact a variety of tissues in a complex manner that regulates inflammation, cell death, and cell proliferation and migration as well as healing mechanisms. Ethanol (alcohol) is known to alter cytokine levels in a variety of tissues including plasma, lung, liver, and brain. Studies on human monocyte responses to pathogens reveal ethanol disruption of cytokine production depending upon the pathogen and duration of alcohol consumption, with multiple pathogens and chronic ethanol promoting inflammatory cytokine production. In lung, cytokine production is disrupted by ethanol exacerbating respiratory distress syndrome with greatly increased expression of transforming growth factor β (TGFβ). Alcoholic liver disease involves an inflammatory hepatitis and an exaggerated Th1 response with increases in tumor necrosis factor α (TNFα). Recent studies suggest that the transition from Th1 to Th2 cytokines contribute to hepatic fibrosis and cirrhosis. Cytokines affect the brain and likely contribute to changes in the central nervous system that contribute to long-term changes in behavior and neurodegeneration. Together these studies suggest that ethanol disruption of cytokines and inflammation contribute in multiple ways to a diversity of alcoholic pathologies.