Alcohol, intestinal bacterial growth, intestinal permeability to endotoxin, and medical consequences: summary of a symposium

Alcohol. 2008 Aug;42(5):349-61. doi: 10.1016/j.alcohol.2008.03.131. Epub 2008 May 27.

Abstract

This report is a summary of the symposium on Alcohol, Intestinal Bacterial Growth, Intestinal Permeability to Endotoxin, and Medical Consequences, organized by National Institute on Alcohol Abuse and Alcoholism, Office of Dietary Supplements, and National Institute of Diabetes and Digestive and Kidney Diseases of National Institutes of Health in Rockville, Maryland, October 11, 2006. Alcohol exposure can promote the growth of Gram-negative bacteria in the intestine, which may result in accumulation of endotoxin. In addition, alcohol metabolism by Gram-negative bacteria and intestinal epithelial cells can result in accumulation of acetaldehyde, which in turn can increase intestinal permeability to endotoxin by increasing tyrosine phosphorylation of tight junction and adherens junction proteins. Alcohol-induced generation of nitric oxide may also contribute to increased permeability to endotoxin by reacting with tubulin, which may cause damage to microtubule cytoskeleton and subsequent disruption of intestinal barrier function. Increased intestinal permeability can lead to increased transfer of endotoxin from the intestine to the liver and general circulation where endotoxin may trigger inflammatory changes in the liver and other organs. Alcohol may also increase intestinal permeability to peptidoglycan, which can initiate inflammatory response in liver and other organs. In addition, acute alcohol exposure may potentiate the effect of burn injury on intestinal bacterial growth and permeability. Decreasing the number of Gram-negative bacteria in the intestine can result in decreased production of endotoxin as well as acetaldehyde which is expected to decrease intestinal permeability to endotoxin. In addition, intestinal permeability may be preserved by administering epidermal growth factor, l-glutamine, oats supplementation, or zinc, thereby preventing the transfer of endotoxin to the general circulation. Thus reducing the number of intestinal Gram-negative bacteria and preserving intestinal permeability to endotoxin may attenuate alcoholic liver and other organ injuries.

Publication types

  • Congress
  • Research Support, N.I.H., Extramural

MeSH terms

  • Acetaldehyde / metabolism
  • Alcohol Drinking / adverse effects*
  • Alcohol Drinking / metabolism
  • Animals
  • Avena / metabolism
  • Bacterial Translocation / drug effects*
  • Burns / metabolism
  • Endotoxins / blood
  • Endotoxins / metabolism*
  • ErbB Receptors / metabolism
  • Ethanol / adverse effects*
  • Glutamine / metabolism
  • Gram-Negative Bacteria / drug effects*
  • Gram-Negative Bacteria / growth & development
  • Gram-Negative Bacteria / metabolism
  • Humans
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / metabolism
  • Intestines / drug effects*
  • Intestines / microbiology
  • Liver Diseases, Alcoholic / etiology
  • Liver Diseases, Alcoholic / metabolism
  • Nitric Oxide / metabolism
  • Permeability
  • Probiotics / therapeutic use
  • Zinc / metabolism

Substances

  • Endotoxins
  • Glutamine
  • Nitric Oxide
  • Ethanol
  • ErbB Receptors
  • Acetaldehyde
  • Zinc