Acetaldehyde-induced barrier disruption and paracellular permeability in Caco-2 cell monolayer.
A significant body of evidence indicates that endotoxemia plays a crucial role in the pathogenesis of alcoholic liver disease. There are several possible factors that may be involved in inducing alcoholic endotoxemia, but increased intestinal permeability to enteric endotoxins appears to be the major contributing factor. In the normal gut, the epithelial barrier function prevents diffusion of toxins across the epithelium. However, the barrier is disrupted in patients with alcoholic liver disease. We showed that acetaldehyde disrupts intestinal epithelial tight junctions and increases paracellular permeability to endotoxins in Caco-2 cell monolayer, the extensively studied model of the differentiated intestinal epithelium. The mechanisms involved in acetaldehyde-induced increase in intestinal permeability to endotoxins can be elucidated in this model of the intestinal epithelium.
Rao
R K
RK
University of Tennessee Health Science Center, Department of Physiology, Memphis, TN, USA.
D000079:Acetaldehyde / Q000378:metabolism / Q000633:toxicity*; D018938:Caco-2 Cells; D018929:Cell Culture Techniques; D002470:Cell Survival / Q000187:drug effects; D017097:Electric Impedance; D004731:Endotoxins / Q000378:metabolism*; D004847:Epithelial Cells / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D000431:Ethanol / Q000378:metabolism / Q000633:toxicity*; D005455:Fluorescent Antibody Technique; D006801:Humans; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D007444:Inulin / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008108:Liver Diseases, Alcoholic / Q000378:metabolism; D018613:Microscopy, Confocal; D010539:Permeability; D019108:Tight Junctions / Q000187:drug effects* / Q000378:metabolism; D013997:Time Factors
D004731:Endotoxins; D000431:Ethanol; D007444:Inulin; D007770:L-Lactate Dehydrogenase; D000079:Acetaldehyde