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Acetaldehyde-induced Barrier Disruption and Paracellular Permeability in Caco-2 Cell Monolayer

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Alcohol

Part of the book series: Methods in Molecular Biology™ ((MIMB,volume 447))

Summary

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.

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Acknowledgements

This work was supported by NIH grant R01 AA12307.

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© 2008 Humana Press, a part of Springer Science+Business Media, LLC

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Rao, R.K. (2008). Acetaldehyde-induced Barrier Disruption and Paracellular Permeability in Caco-2 Cell Monolayer. In: Nagy, L.E. (eds) Alcohol. Methods in Molecular Biology™, vol 447. Humana Press. https://doi.org/10.1007/978-1-59745-242-7_13

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  • DOI: https://doi.org/10.1007/978-1-59745-242-7_13

  • Publisher Name: Humana Press

  • Print ISBN: 978-1-58829-906-2

  • Online ISBN: 978-1-59745-242-7

  • eBook Packages: Springer Protocols

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