Interleukin-30: A novel antiinflammatory cytokine candidate for prevention and treatment of inflammatory cytokine-induced liver injury
The liver is the major metabolic organ and is subjected to constant attacks from chronic viral infection, uptake of therapeutic drugs, life behavior (alcoholic), and environmental contaminants, all of which result in chronic inflammation, fibrosis, and, ultimately, cancer. Therefore, there is an urg...
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| Published in | Hepatology (Baltimore, Md.) Vol. 55; no. 4; pp. 1204 - 1214 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.04.2012
Wiley Wolters Kluwer Health, Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | The liver is the major metabolic organ and is subjected to constant attacks from chronic viral infection, uptake of therapeutic drugs, life behavior (alcoholic), and environmental contaminants, all of which result in chronic inflammation, fibrosis, and, ultimately, cancer. Therefore, there is an urgent need to discover effective therapeutic agents for the prevention and treatment of liver injury, the ideal drug being a naturally occurring biological inhibitor. Here we establish the role of IL30 as a potent antiinflammatory cytokine that can inhibit inflammation‐induced liver injury. In contrast, interleukin (IL)27, which contains IL30 as a subunit, is not hepatoprotective. Interestingly, IL30 is induced by the proinflammatory signal such as IL12 through interferon‐gamma (IFN‐γ) / signal transducer and activator of transcription 1 signaling. In animal models, administration of IL30 by way of a gene therapy approach prevents and treats both IL12‐, IFN‐γ‐, and concanavalin A‐induced liver toxicity. Likewise, immunohistochemistry analysis of human tissue samples revealed that IL30 is highly expressed in hepatocytes, yet barely expressed in inflammation‐induced tissue such as fibrous/connective tissue. Conclusion: These novel observations reveal a novel role of IL30 as a therapeutic cytokine that suppresses proinflammatory cytokine‐associated liver toxicity. (Hepatology 2012) |
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| AbstractList | The liver is the major metabolic organ and is subjected to constant attacks from chronic viral infection, uptake of therapeutic drugs, life behavior (alcoholic), and environmental contaminants, all of which result in chronic inflammation, fibrosis, and, ultimately, cancer. Therefore, there is an urgent need to discover effective therapeutic agents for the prevention and treatment of liver injury, the ideal drug being a naturally occurring biological inhibitor. Here we establish the role of IL30 as a potent antiinflammatory cytokine that can inhibit inflammation-induced liver injury. In contrast, interleukin (IL)27, which contains IL30 as a subunit, is not hepatoprotective. Interestingly, IL30 is induced by the proinflammatory signal such as IL12 through interferon-gamma (IFN- gamma ) / signal transducer and activator of transcription 1 signaling. In animal models, administration of IL30 by way of a gene therapy approach prevents and treats both IL12-, IFN- gamma -, and concanavalin A-induced liver toxicity. Likewise, immunohistochemistry analysis of human tissue samples revealed that IL30 is highly expressed in hepatocytes, yet barely expressed in inflammation-induced tissue such as fibrous/connective tissue. Conclusion: These novel observations reveal a novel role of IL30 as a therapeutic cytokine that suppresses proinflammatory cytokine-associated liver toxicity. (Hepatology 2012) The liver is the major metabolic organ and is subjected to constant attacks from chronic viral infection, uptake of therapeutic drugs, life behavior (alcoholic), and environmental contaminants, all of which result in chronic inflammation, fibrosis, and, ultimately, cancer. Therefore, there is an urgent need to discover effective therapeutic agents for the prevention and treatment of liver injury, the ideal drug being a naturally occurring biological inhibitor. Here we establish the role of IL30 as a potent antiinflammatory cytokine that can inhibit inflammation-induced liver injury. In contrast, interleukin (IL)27, which contains IL30 as a subunit, is not hepatoprotective. Interestingly, IL30 is induced by the proinflammatory signal such as IL12 through interferon-gamma (IFN-γ)/signal transducer and activator of transcription 1 signaling. In animal models, administration of IL30 by way of a gene therapy approach prevents and treats both IL12-, IFN-γ-, and concanavalin A-induced liver toxicity. Likewise, immunohistochemistry analysis of human tissue samples revealed that IL30 is highly expressed in hepatocytes, yet barely expressed in inflammation-induced tissue such as fibrous/connective tissue.UNLABELLEDThe liver is the major metabolic organ and is subjected to constant attacks from chronic viral infection, uptake of therapeutic drugs, life behavior (alcoholic), and environmental contaminants, all of which result in chronic inflammation, fibrosis, and, ultimately, cancer. Therefore, there is an urgent need to discover effective therapeutic agents for the prevention and treatment of liver injury, the ideal drug being a naturally occurring biological inhibitor. Here we establish the role of IL30 as a potent antiinflammatory cytokine that can inhibit inflammation-induced liver injury. In contrast, interleukin (IL)27, which contains IL30 as a subunit, is not hepatoprotective. Interestingly, IL30 is induced by the proinflammatory signal such as IL12 through interferon-gamma (IFN-γ)/signal transducer and activator of transcription 1 signaling. In animal models, administration of IL30 by way of a gene therapy approach prevents and treats both IL12-, IFN-γ-, and concanavalin A-induced liver toxicity. Likewise, immunohistochemistry analysis of human tissue samples revealed that IL30 is highly expressed in hepatocytes, yet barely expressed in inflammation-induced tissue such as fibrous/connective tissue.These novel observations reveal a novel role of IL30 as a therapeutic cytokine that suppresses proinflammatory cytokine-associated liver toxicity.CONCLUSIONThese novel observations reveal a novel role of IL30 as a therapeutic cytokine that suppresses proinflammatory cytokine-associated liver toxicity. The liver is the major metabolic organ and is subjected to constant attacks from chronic viral infection, uptake of therapeutic drugs, life behavior (alcoholic), and environmental contaminants, all of which result in chronic inflammation, fibrosis, and, ultimately, cancer. Therefore, there is an urgent need to discover effective therapeutic agents for the prevention and treatment of liver injury, the ideal drug being a naturally occurring biological inhibitor. Here we establish the role of IL30 as a potent antiinflammatory cytokine that can inhibit inflammation‐induced liver injury. In contrast, interleukin (IL)27, which contains IL30 as a subunit, is not hepatoprotective. Interestingly, IL30 is induced by the proinflammatory signal such as IL12 through interferon‐gamma (IFN‐γ) / signal transducer and activator of transcription 1 signaling. In animal models, administration of IL30 by way of a gene therapy approach prevents and treats both IL12‐, IFN‐γ‐, and concanavalin A‐induced liver toxicity. Likewise, immunohistochemistry analysis of human tissue samples revealed that IL30 is highly expressed in hepatocytes, yet barely expressed in inflammation‐induced tissue such as fibrous/connective tissue. Conclusion: These novel observations reveal a novel role of IL30 as a therapeutic cytokine that suppresses proinflammatory cytokine‐associated liver toxicity. (Hepatology 2012) The liver is the major metabolic organ and is subjected to constant attacks from chronic viral infection, uptake of therapeutic drugs, life behavior (alcoholic), and environmental contaminants, all of which result in chronic inflammation, fibrosis, and, ultimately, cancer. Therefore, there is an urgent need to discover effective therapeutic agents for the prevention and treatment of liver injury, the ideal drug being a naturally occurring biological inhibitor. Here we establish the role of IL30 as a potent antiinflammatory cytokine that can inhibit inflammation-induced liver injury. In contrast, interleukin (IL)27, which contains IL30 as a subunit, is not hepatoprotective. Interestingly, IL30 is induced by the proinflammatory signal such as IL12 through interferon-gamma (IFN-γ)/signal transducer and activator of transcription 1 signaling. In animal models, administration of IL30 by way of a gene therapy approach prevents and treats both IL12-, IFN-γ-, and concanavalin A-induced liver toxicity. Likewise, immunohistochemistry analysis of human tissue samples revealed that IL30 is highly expressed in hepatocytes, yet barely expressed in inflammation-induced tissue such as fibrous/connective tissue. These novel observations reveal a novel role of IL30 as a therapeutic cytokine that suppresses proinflammatory cytokine-associated liver toxicity. |
| Author | Cutrera, Jeffry Dibra, Denada Kallakury, Bhaskar Mishra, Lopa Li, Shulin Xia, Xueqing |
| Author_xml | – sequence: 1 givenname: Denada surname: Dibra fullname: Dibra, Denada organization: Department of Pediatrics Research, University of Texas MD Anderson Cancer Center, Houston, TX – sequence: 2 givenname: Jeffry surname: Cutrera fullname: Cutrera, Jeffry organization: Department of Pediatrics Research, University of Texas MD Anderson Cancer Center, Houston, TX – sequence: 3 givenname: Xueqing surname: Xia fullname: Xia, Xueqing organization: Department of Pediatrics Research, University of Texas MD Anderson Cancer Center, Houston, TX – sequence: 4 givenname: Bhaskar surname: Kallakury fullname: Kallakury, Bhaskar organization: Department of Pathology, Georgetown University Hospital, Washington, DC – sequence: 5 givenname: Lopa surname: Mishra fullname: Mishra, Lopa organization: Department of Gastroenterology, Hepatology and Nutrition, University of Texas MD Anderson Cancer Center, Houston, TX – sequence: 6 givenname: Shulin surname: Li fullname: Li, Shulin email: sli4@mdanderson.org organization: Department of Pediatrics Research, University of Texas MD Anderson Cancer Center, Houston, TX |
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| Copyright | Copyright © 2011 American Association for the Study of Liver Diseases 2015 INIST-CNRS Copyright © 2011 American Association for the Study of Liver Diseases. |
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| Keywords | Prevention Treatment Liver Interleukin Antiinflammatory agent Cytokine Gastroenterology |
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| SubjectTerms | Animals Biological and medical sciences Bones, joints and connective tissue. Antiinflammatory agents Chemical and Drug Induced Liver Injury - prevention & control Chemical and Drug Induced Liver Injury - therapy Concanavalin A - adverse effects Cytokines Cytokines - adverse effects Disease Models, Animal Gastroenterology. Liver. Pancreas. Abdomen Genetic Therapy Hepatology Humans In Vitro Techniques Inflammation Interferon-gamma - adverse effects Interferon-gamma - metabolism Interleukin-12 - adverse effects Interleukin-12 - genetics Interleukin-12 - metabolism Interleukins - genetics Interleukins - metabolism Liver Liver - metabolism Liver - pathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Medical sciences Mice Mice, Inbred BALB C Mice, Inbred C3H Mice, Inbred C57BL Mice, Knockout Minor Histocompatibility Antigens Pharmacology. Drug treatments Receptors, Cytokine - deficiency Receptors, Cytokine - genetics Receptors, Interleukin STAT1 Transcription Factor - deficiency STAT1 Transcription Factor - genetics |
| Title | Interleukin-30: A novel antiinflammatory cytokine candidate for prevention and treatment of inflammatory cytokine-induced liver injury |
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