The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.
Interleukin-22 Treatment Ameliorates Alcoholic Liver Injury in a Murine Model of Chronic-Binge Ethanol Feeding: Role of Signal Transducer and Activator of Transcription 3
Open accessAbstract
Interleukin-22 (IL-22), a recently identified member of the IL-10 family of cytokines that is produced by Th17 and natural killer cells, plays an important role in controlling bacterial infection, homeostasis, and tissue repair. Here, we tested the effect of IL-22 on alcohol-induced liver injury in a murine model of chronic-binge ethanol feeding. Feeding male C57BL/6 mice with a Lieber-DeCarli diet containing 5% ethanol for 10 days, followed by a single dose of ethanol (5 g/kg body weight) by gavage, induces significant fatty liver and liver injury with peak serum levels of approximately 250 IU/L alanine aminotransferase and 420 IU/L aspartate aminotransferase 9 hours after gavage. Moreover, chronic-binge ethanol administration increases expression of hepatic and serum inflammatory cytokines and hepatic oxidative stress. Using this model, we demonstrate that treatment with IL-22 recombinant protein activates hepatic signal transducer and activator of transcription 3 (STAT3) and ameliorates alcoholic fatty liver, liver injury, and hepatic oxidative stress. Administration with IL-22 adenovirus also prevents alcohol-induced steatosis and liver injury. Deletion of STAT3 in hepatocytes abolishes the hepatoprotection provided by IL-22 in alcoholic liver injury. In addition, IL-22 treatment down-regulates the hepatic expression of fatty acid transport protein, but up-regulates several antioxidant, antiapoptotic, and antimicrobial genes. Finally, expression of IL-22 receptor 1 is up-regulated whereas IL-22 is undetectable in the livers from mice with chronic-binge ethanol feeding or patients with alcoholic hepatitis. Conclusion: Chronic-binge ethanol feeding may be a useful model to study the early stages of alcoholic liver injury. IL-22 treatment could be a potential therapeutic option to ameliorate alcoholic liver disease, due to its antioxidant, antiapoptotic, antisteatotic, proliferative, and antimicrobial effects with the added benefit of potentially few side effects. Hepatology 2010
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Cites
O'Shea, R. S., Dasarathy, S., & McCullough, A. J. (2010) · Hepatology · doi:10.1002/hep.23258 · Cited by 1,077
Lucey, M. R., Mathurin, P., & Morgan, T. R. (2009) · New England Journal of Medicine · doi:10.1056/nejmra0805786 · Cited by 863
Radaeva, S., Sun, R., Pan, H.-N., Hong, F., & Gao, B. (2004) · Hepatology · doi:10.1002/hep.20184 · Cited by 597
Self-citationNaveau, S., Chollet-Martin, S., Dharancy, S., Mathurin, P., Jouet, P., Piquet, M.-A., Davion, T., Oberti, F., Broët, P., & Emilie, D. (2004) · Hepatology · doi:10.1002/hep.20206 · Cited by 446
Hritz, I., Mandrekar, P., Velayudham, A., Catalano, D., Dolganiuc, A., Kodys, K., Kurt‐Jones, E., & Szabo, G. (2008) · Hepatology · doi:10.1002/hep.22470 · Cited by 415
Antibodies to tumor necrosis factor-alpha inhibit liver regeneration after partial hepatectomy
Akerman, P., Cote, P., Yang, S. Q., McClain, C., Nelson, S., Bagby, G. J., & Diehl, A. M. (1992) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.1992.263.4.g579 · Cited by 401
Wolk, K., Witte, E., Witte, K., Warszawska, K., & Sabat, R. (2010) · Seminars in Immunopathology · doi:10.1007/s00281-009-0188-x · Cited by 395
The interleukin-17 pathway is involved in human alcoholic liver disease # †
Lemmers, A., Moreno, C., Gustot, T., Maréchal, R., Degré, D., Demetter, P., de Nadai, P., Geerts, A., Quertinmont, E., Vercruysse, V., et al. (2009) · Hepatology · doi:10.1002/hep.22680 · Cited by 394
Louvet, A., Wartel, F., Castel, H., Dharancy, S., Hollebecque, A., Canva–Delcambre, V., Deltenre, P., & Mathurin, P. (2009) · Gastroenterology · doi:10.1053/j.gastro.2009.04.062 · Cited by 367
Boetticher, N. C., Peine, C. J., Kwo, P., Abrams, G. A., Patel, T., Aqel, B., Boardman, L., Gores, G. J., Harmsen, W. S., McClain, C. J., et al. (2008) · Gastroenterology · doi:10.1053/j.gastro.2008.08.057 · Cited by 340
Cited by
Molecular and cellular mechanisms of liver fibrosis and its regression
Kisseleva, T., & Brenner, D. (2021) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-020-00372-7 · Cited by 2,024
Alcoholic Liver Disease: Pathogenesis and New Therapeutic Targets
Gao, B., & Bataller, R. (2011) · Gastroenterology · doi:10.1053/j.gastro.2011.09.002 · Cited by 1,963
Self-citationInterleukin-22: Immunobiology and Pathology
Dudakov, J. A., Hanash, A. M., & van den Brink, M. R. M. (2015) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032414-112123 · Cited by 905
Gut–Liver Axis in Alcoholic Liver Disease
Szabo, G. (2015) · Gastroenterology · doi:10.1053/j.gastro.2014.10.042 · Cited by 754
Intestinal Barrier in Human Health and Disease
Di Tommaso, N., Gasbarrini, A., & Ponziani, F. R. (2021) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph182312836 · Cited by 533
Metadata
- Authors
- Ki, S. H., Park, O., Zheng, M., Morales-Ibanez, O., Kolls, J. K., Bataller, R., & Gao, B.
- Venue
- Hepatology
- Published
- 2010-10
- Volume
- 52
- Issue
- 4
- Pages
- 1291-1300
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W2062564526
- Cited by
- 434
- References
- 39
- FWCI
- 15.77
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Ki, S. H., Park, O., Zheng, M., Morales-Ibanez, O., Kolls, J. K., Bataller, R., & Gao, B. (2010). Interleukin-22 Treatment Ameliorates Alcoholic Liver Injury in a Murine Model of Chronic-Binge Ethanol Feeding: Role of Signal Transducer and Activator of Transcription 3. Hepatology. https://doi.org/10.1002/hep.23837
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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