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In vivo consequences of liver-specific interleukin-22 expression in mice: implications for human liver disease progression

Interleukin-22 (IL-22), which acts as either a proinflammatory or anti-inflammatory cytokine in various disease models, is markedly up-regulated in chronic liver diseases, including hepatitis B and C. In this report, we demonstrate a strong correlation between IL-22 expression in the liver with acti...

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Hauptverfasser: Park, Ogyi (VerfasserIn) , Wang, Hua (VerfasserIn) , Weng, Honglei (VerfasserIn) , Feigenbaum, Lionel (VerfasserIn) , Li, Hai (VerfasserIn) , Yin, Shi (VerfasserIn) , Ki, Sung Hwan (VerfasserIn) , Yoo, Seong Ho (VerfasserIn) , Dooley, Steven (VerfasserIn) , Wang, Fu-Sheng (VerfasserIn) , Young, Howard A. (VerfasserIn) , Gao, Bin (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 4 April 2011
In: Hepatology
Year: 2011, Jahrgang: 54, Heft: 1, Pages: 252-261
ISSN:1527-3350
DOI:10.1002/hep.24339
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1002/hep.24339
Volltext
Verfasserangaben:Ogyi Park, Hua Wang, Honglei Weng, Lionel Feigenbaum, Hai Li, Shi Yin, Sung Hwan Ki, Seong Ho Yoo, Steven Dooley, Fu-Sheng Wang, Howard A. Young, and Bin Gao
Beschreibung
Zusammenfassung:Interleukin-22 (IL-22), which acts as either a proinflammatory or anti-inflammatory cytokine in various disease models, is markedly up-regulated in chronic liver diseases, including hepatitis B and C. In this report, we demonstrate a strong correlation between IL-22 expression in the liver with active, inflammatory human liver disease. To clarify the role of IL-22 up-regulation in the pathogenesis of liver diseases, liver-specific IL-22 transgenic (IL-22TG) mice, under the control of albumin promoter, were developed. Despite elevated IL-22 serum levels ranging from 4,000 to 7,000 pg/mL, IL-22TG mice developed normally without obvious adverse phenotypes or evidence of chronic inflammation (except for slightly thicker epidermis and minor inflammation of the skin) compared with wild-type mice. Interestingly, IL-22TG mice were completely resistant to concanavalin A-induced T cell hepatitis with minimal effect on liver inflammation and had accelerated liver regeneration after partial hepatectomy. Although they did not spontaneously develop liver tumors, IL-22TG mice were more susceptible to diethylnitrosamine-induced liver cancer. Microarray analyses revealed that a variety of antioxidant, mitogenic, acute phase genes were up-regulated in the livers of IL-22TG mice compared with those from wild-type mice. - CONCLUSION: These findings indicate that localized production of IL-22 in the liver promotes hepatocyte survival and proliferation but primes the liver to be more susceptible to tumor development without significantly affecting liver inflammation.
Beschreibung:Gesehen am 09.09.2022
Beschreibung:Online Resource
ISSN:1527-3350
DOI:10.1002/hep.24339

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