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

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

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..

Medienart:	E-Artikel

Erscheinungsjahr:	4 April 2011 2011
Erschienen:	4 April 2011

Enthalten in:	Zur Gesamtaufnahme - volume:54
Enthalten in:	Hepatology - 54(2011), 1, Seite 252-261

Sprache:	Englisch

Beteiligte Personen:	Park, Ogyi [VerfasserIn] Wang, Hua [VerfasserIn] Weng, Honglei, 1969- [VerfasserIn] Feigenbaum, Lionel [VerfasserIn] Li, Hai [VerfasserIn] Yin, Shi [VerfasserIn] Ki, Sung Hwan [VerfasserIn] Yoo, Seong Ho [VerfasserIn] Dooley, Steven, 1960- [VerfasserIn] Wang, Fu-Sheng [VerfasserIn] Young, Howard A. [VerfasserIn] Gao, Bin [VerfasserIn]

Links:	Volltext [lizenzpflichtig]

Themen:	Animals Cell Survival Chemical and Drug Induced Liver Injury, Chronic Concanavalin A Diethylnitrosamine Disease Models, Animal Disease Progression Hepatectomy Hepatitis B Hepatitis C Humans Interleukins Liver Liver Diseases Liver Neoplasms Liver Regeneration Mice Mice, Inbred C57BL Mice, Transgenic

Anmerkungen:	Gesehen am 09.09.2022

Umfang:	10

doi:	10.1002/hep.24339

funding:
Förderinstitution / Projekttitel:

PPN (Katalog-ID):	1816370878

Internformat


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245	1	0	\|a In vivo consequences of liver-specific interleukin-22 expression in mice \|b implications for human liver disease progression \|c 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
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520			\|a 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.
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650		4	\|a Concanavalin A
650		4	\|a Diethylnitrosamine
650		4	\|a Disease Models, Animal
650		4	\|a Disease Progression
650		4	\|a Hepatectomy
650		4	\|a Hepatitis B
650		4	\|a Hepatitis C
650		4	\|a Humans
650		4	\|a Interleukins
650		4	\|a Liver
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650		4	\|a Liver Neoplasms
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650		4	\|a Mice
650		4	\|a Mice, Inbred C57BL
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In vivo consequences of liver-specific interleukin-22 expression in mice : implications for human liver disease progression / 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

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