In vivo consequences of liver-specific interleukin-22 expression in mice

• Verfasst von: Park, Ogyi [VerfasserIn]
• Verfasst von: Wang, Hua [VerfasserIn]
• Verfasst von: Weng, Honglei [VerfasserIn]
• Verfasst von: Feigenbaum, Lionel [VerfasserIn]
• Verfasst von: Li, Hai [VerfasserIn]
• Verfasst von: Yin, Shi [VerfasserIn]
• Verfasst von: Ki, Sung Hwan [VerfasserIn]
• Verfasst von: Yoo, Seong Ho [VerfasserIn]
• Verfasst von: Dooley, Steven [VerfasserIn]
• Verfasst von: Wang, Fu-Sheng [VerfasserIn]
• Verfasst von: Young, Howard A. [VerfasserIn]
• Verfasst von: Gao, Bin [VerfasserIn]
• Titel: In vivo consequences of liver-specific interleukin-22 expression in mice
• Titelzusatz: implications for human liver disease progression
• Verf.angabe: 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
• E-Jahr: 2011
• Jahr: 4 April 2011
• Umfang: 10 S.
• Fussnoten: Gesehen am 09.09.2022
• Titel Quelle: Enthalten in: Hepatology
• Ort Quelle: [Alphen aan den Rijn] : Wolters Kluwer Health, 1981
• Jahr Quelle: 2011
• Band/Heft Quelle: 54(2011), 1, Seite 252-261
• ISSN Quelle: 1527-3350
• DOI: doi:10.1002/hep.24339
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Animals
• Sach-SW: Cell Survival
• Sach-SW: Chemical and Drug Induced Liver Injury, Chronic
• Sach-SW: Concanavalin A
• Sach-SW: Diethylnitrosamine
• Sach-SW: Disease Models, Animal
• Sach-SW: Disease Progression
• Sach-SW: Hepatectomy
• Sach-SW: Hepatitis B
• Sach-SW: Hepatitis C
• Sach-SW: Humans
• Sach-SW: Interleukins
• Sach-SW: Liver
• Sach-SW: Liver Diseases
• Sach-SW: Liver Neoplasms
• Sach-SW: Liver Regeneration
• Sach-SW: Mice
• Sach-SW: Mice, Inbred C57BL
• Sach-SW: Mice, Transgenic
• K10plus-PPN: 1816370878

Abstract

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.