Interleukin-17 Signaling in Inflammatory, Kupffer Cells, and Hepatic Stellate Cells Exacerbates Liver Fibrosis in Mice
Background & Aims: Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.Methods: Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis i...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Meng, Fanli [verfasserIn] Wang, Kai [verfasserIn] Aoyama, Tomonori [verfasserIn] Grivennikov, Sergei I. [verfasserIn] Paik, YongHan [verfasserIn] Scholten, David [verfasserIn] Cong, Min [verfasserIn] Iwaisako, Keiko [verfasserIn] Liu, Xiao [verfasserIn] Zhang, Mingjun [verfasserIn] Österreicher, Christoph H. [verfasserIn] Stickel, Felix [verfasserIn] Ley, Klaus [verfasserIn] Brenner, David A. [verfasserIn] Kisseleva, Tatiana [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2012 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Gastroenterology - Stanford, Calif. : HighWire Press, 1965, 143 |
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| Übergeordnetes Werk: |
volume:143 |
| DOI / URN: |
10.1053/j.gastro.2012.05.049 |
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ELV002120313 |
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| 024 | 7 | |a 10.1053/j.gastro.2012.05.049 |2 doi | |
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| 100 | 1 | |a Meng, Fanli |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Interleukin-17 Signaling in Inflammatory, Kupffer Cells, and Hepatic Stellate Cells Exacerbates Liver Fibrosis in Mice |
| 264 | 1 | |c 2012 | |
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| 520 | |a Background & Aims: Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.Methods: Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis in wild-type mice with that of IL-17RA −/− mice and of bone marrow chimeric mice devoid of IL-17 signaling in immune and Kupffer cells (IL-17RA −/− to wild-type and IL-17A −/− to wild-type mice) or liver resident cells (wild-type to IL-17RA −/− mice).Results: In response to liver injury, levels of Il-17A and its receptor increased. IL-17A increased appeared to promote fibrosis by activating inflammatory and liver resident cells. IL-17 signaling facilitated production of IL-6, IL-1, and tumor necrosis factor-α by inflammatory cells and increased the expression of transforming growth factor-1, a fibrogenic cytokine. IL-17 directly induced production of collagen type I in hepatic stellate cells by activating the signal transducer and activator of transcription 3 (Stat3) signaling pathway. Mice devoid of Stat3 signaling in hepatic stellate cells (GFAPStat3 −/− mice) were less susceptible to fibrosis. Furthermore, deletion of IL-23 from immune cells attenuated liver fibrosis, whereas deletion of IL-22 exacerbated fibrosis. Administration of IL-22 and IL-17E (IL-25, a negative regulator of IL-23) protected mice from bile duct ligation-induced liver fibrosis.Conclusions: IL-17 induces liver fibrosis through multiple mechanisms in mice. Reagents that block these pathways might be developed as therapeutics for patients with cirrhosis. | ||
| 650 | 4 | |a Mouse Model | |
| 650 | 4 | |a Immune Response | |
| 650 | 4 | |a Bone Marrow-Derived Macrophages | |
| 650 | 4 | |a Myofibroblast | |
| 700 | 1 | |a Wang, Kai |e verfasserin |4 aut | |
| 700 | 1 | |a Aoyama, Tomonori |e verfasserin |4 aut | |
| 700 | 1 | |a Grivennikov, Sergei I. |e verfasserin |4 aut | |
| 700 | 1 | |a Paik, YongHan |e verfasserin |4 aut | |
| 700 | 1 | |a Scholten, David |e verfasserin |4 aut | |
| 700 | 1 | |a Cong, Min |e verfasserin |4 aut | |
| 700 | 1 | |a Iwaisako, Keiko |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Xiao |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Mingjun |e verfasserin |4 aut | |
| 700 | 1 | |a Österreicher, Christoph H. |e verfasserin |4 aut | |
| 700 | 1 | |a Stickel, Felix |e verfasserin |4 aut | |
| 700 | 1 | |a Ley, Klaus |e verfasserin |4 aut | |
| 700 | 1 | |a Brenner, David A. |e verfasserin |4 aut | |
| 700 | 1 | |a Kisseleva, Tatiana |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Gastroenterology |d Stanford, Calif. : HighWire Press, 1965 |g 143 |h Online-Ressource |w (DE-627)270937293 |w (DE-600)1478699-0 |w (DE-576)078590221 |x 1528-0012 |7 nnns |
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2012 |
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2012 |
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10.1053/j.gastro.2012.05.049 doi (DE-627)ELV002120313 (ELSEVIER)S0016-5085(12)00817-7 DE-627 ger DE-627 rda eng 610 DE-600 44.87 bkl Meng, Fanli verfasserin aut Interleukin-17 Signaling in Inflammatory, Kupffer Cells, and Hepatic Stellate Cells Exacerbates Liver Fibrosis in Mice 2012 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background & Aims: Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.Methods: Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis in wild-type mice with that of IL-17RA −/− mice and of bone marrow chimeric mice devoid of IL-17 signaling in immune and Kupffer cells (IL-17RA −/− to wild-type and IL-17A −/− to wild-type mice) or liver resident cells (wild-type to IL-17RA −/− mice).Results: In response to liver injury, levels of Il-17A and its receptor increased. IL-17A increased appeared to promote fibrosis by activating inflammatory and liver resident cells. IL-17 signaling facilitated production of IL-6, IL-1, and tumor necrosis factor-α by inflammatory cells and increased the expression of transforming growth factor-1, a fibrogenic cytokine. IL-17 directly induced production of collagen type I in hepatic stellate cells by activating the signal transducer and activator of transcription 3 (Stat3) signaling pathway. Mice devoid of Stat3 signaling in hepatic stellate cells (GFAPStat3 −/− mice) were less susceptible to fibrosis. Furthermore, deletion of IL-23 from immune cells attenuated liver fibrosis, whereas deletion of IL-22 exacerbated fibrosis. Administration of IL-22 and IL-17E (IL-25, a negative regulator of IL-23) protected mice from bile duct ligation-induced liver fibrosis.Conclusions: IL-17 induces liver fibrosis through multiple mechanisms in mice. Reagents that block these pathways might be developed as therapeutics for patients with cirrhosis. Mouse Model Immune Response Bone Marrow-Derived Macrophages Myofibroblast Wang, Kai verfasserin aut Aoyama, Tomonori verfasserin aut Grivennikov, Sergei I. verfasserin aut Paik, YongHan verfasserin aut Scholten, David verfasserin aut Cong, Min verfasserin aut Iwaisako, Keiko verfasserin aut Liu, Xiao verfasserin aut Zhang, Mingjun verfasserin aut Österreicher, Christoph H. verfasserin aut Stickel, Felix verfasserin aut Ley, Klaus verfasserin aut Brenner, David A. verfasserin aut Kisseleva, Tatiana verfasserin aut Enthalten in Gastroenterology Stanford, Calif. : HighWire Press, 1965 143 Online-Ressource (DE-627)270937293 (DE-600)1478699-0 (DE-576)078590221 1528-0012 nnns volume:143 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.87 Gastroenterologie AR 143 |
| spelling |
10.1053/j.gastro.2012.05.049 doi (DE-627)ELV002120313 (ELSEVIER)S0016-5085(12)00817-7 DE-627 ger DE-627 rda eng 610 DE-600 44.87 bkl Meng, Fanli verfasserin aut Interleukin-17 Signaling in Inflammatory, Kupffer Cells, and Hepatic Stellate Cells Exacerbates Liver Fibrosis in Mice 2012 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background & Aims: Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.Methods: Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis in wild-type mice with that of IL-17RA −/− mice and of bone marrow chimeric mice devoid of IL-17 signaling in immune and Kupffer cells (IL-17RA −/− to wild-type and IL-17A −/− to wild-type mice) or liver resident cells (wild-type to IL-17RA −/− mice).Results: In response to liver injury, levels of Il-17A and its receptor increased. IL-17A increased appeared to promote fibrosis by activating inflammatory and liver resident cells. IL-17 signaling facilitated production of IL-6, IL-1, and tumor necrosis factor-α by inflammatory cells and increased the expression of transforming growth factor-1, a fibrogenic cytokine. IL-17 directly induced production of collagen type I in hepatic stellate cells by activating the signal transducer and activator of transcription 3 (Stat3) signaling pathway. Mice devoid of Stat3 signaling in hepatic stellate cells (GFAPStat3 −/− mice) were less susceptible to fibrosis. Furthermore, deletion of IL-23 from immune cells attenuated liver fibrosis, whereas deletion of IL-22 exacerbated fibrosis. Administration of IL-22 and IL-17E (IL-25, a negative regulator of IL-23) protected mice from bile duct ligation-induced liver fibrosis.Conclusions: IL-17 induces liver fibrosis through multiple mechanisms in mice. Reagents that block these pathways might be developed as therapeutics for patients with cirrhosis. Mouse Model Immune Response Bone Marrow-Derived Macrophages Myofibroblast Wang, Kai verfasserin aut Aoyama, Tomonori verfasserin aut Grivennikov, Sergei I. verfasserin aut Paik, YongHan verfasserin aut Scholten, David verfasserin aut Cong, Min verfasserin aut Iwaisako, Keiko verfasserin aut Liu, Xiao verfasserin aut Zhang, Mingjun verfasserin aut Österreicher, Christoph H. verfasserin aut Stickel, Felix verfasserin aut Ley, Klaus verfasserin aut Brenner, David A. verfasserin aut Kisseleva, Tatiana verfasserin aut Enthalten in Gastroenterology Stanford, Calif. : HighWire Press, 1965 143 Online-Ressource (DE-627)270937293 (DE-600)1478699-0 (DE-576)078590221 1528-0012 nnns volume:143 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.87 Gastroenterologie AR 143 |
| allfields_unstemmed |
10.1053/j.gastro.2012.05.049 doi (DE-627)ELV002120313 (ELSEVIER)S0016-5085(12)00817-7 DE-627 ger DE-627 rda eng 610 DE-600 44.87 bkl Meng, Fanli verfasserin aut Interleukin-17 Signaling in Inflammatory, Kupffer Cells, and Hepatic Stellate Cells Exacerbates Liver Fibrosis in Mice 2012 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background & Aims: Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.Methods: Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis in wild-type mice with that of IL-17RA −/− mice and of bone marrow chimeric mice devoid of IL-17 signaling in immune and Kupffer cells (IL-17RA −/− to wild-type and IL-17A −/− to wild-type mice) or liver resident cells (wild-type to IL-17RA −/− mice).Results: In response to liver injury, levels of Il-17A and its receptor increased. IL-17A increased appeared to promote fibrosis by activating inflammatory and liver resident cells. IL-17 signaling facilitated production of IL-6, IL-1, and tumor necrosis factor-α by inflammatory cells and increased the expression of transforming growth factor-1, a fibrogenic cytokine. IL-17 directly induced production of collagen type I in hepatic stellate cells by activating the signal transducer and activator of transcription 3 (Stat3) signaling pathway. Mice devoid of Stat3 signaling in hepatic stellate cells (GFAPStat3 −/− mice) were less susceptible to fibrosis. Furthermore, deletion of IL-23 from immune cells attenuated liver fibrosis, whereas deletion of IL-22 exacerbated fibrosis. Administration of IL-22 and IL-17E (IL-25, a negative regulator of IL-23) protected mice from bile duct ligation-induced liver fibrosis.Conclusions: IL-17 induces liver fibrosis through multiple mechanisms in mice. Reagents that block these pathways might be developed as therapeutics for patients with cirrhosis. Mouse Model Immune Response Bone Marrow-Derived Macrophages Myofibroblast Wang, Kai verfasserin aut Aoyama, Tomonori verfasserin aut Grivennikov, Sergei I. verfasserin aut Paik, YongHan verfasserin aut Scholten, David verfasserin aut Cong, Min verfasserin aut Iwaisako, Keiko verfasserin aut Liu, Xiao verfasserin aut Zhang, Mingjun verfasserin aut Österreicher, Christoph H. verfasserin aut Stickel, Felix verfasserin aut Ley, Klaus verfasserin aut Brenner, David A. verfasserin aut Kisseleva, Tatiana verfasserin aut Enthalten in Gastroenterology Stanford, Calif. : HighWire Press, 1965 143 Online-Ressource (DE-627)270937293 (DE-600)1478699-0 (DE-576)078590221 1528-0012 nnns volume:143 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.87 Gastroenterologie AR 143 |
| allfieldsGer |
10.1053/j.gastro.2012.05.049 doi (DE-627)ELV002120313 (ELSEVIER)S0016-5085(12)00817-7 DE-627 ger DE-627 rda eng 610 DE-600 44.87 bkl Meng, Fanli verfasserin aut Interleukin-17 Signaling in Inflammatory, Kupffer Cells, and Hepatic Stellate Cells Exacerbates Liver Fibrosis in Mice 2012 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background & Aims: Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.Methods: Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis in wild-type mice with that of IL-17RA −/− mice and of bone marrow chimeric mice devoid of IL-17 signaling in immune and Kupffer cells (IL-17RA −/− to wild-type and IL-17A −/− to wild-type mice) or liver resident cells (wild-type to IL-17RA −/− mice).Results: In response to liver injury, levels of Il-17A and its receptor increased. IL-17A increased appeared to promote fibrosis by activating inflammatory and liver resident cells. IL-17 signaling facilitated production of IL-6, IL-1, and tumor necrosis factor-α by inflammatory cells and increased the expression of transforming growth factor-1, a fibrogenic cytokine. IL-17 directly induced production of collagen type I in hepatic stellate cells by activating the signal transducer and activator of transcription 3 (Stat3) signaling pathway. Mice devoid of Stat3 signaling in hepatic stellate cells (GFAPStat3 −/− mice) were less susceptible to fibrosis. Furthermore, deletion of IL-23 from immune cells attenuated liver fibrosis, whereas deletion of IL-22 exacerbated fibrosis. Administration of IL-22 and IL-17E (IL-25, a negative regulator of IL-23) protected mice from bile duct ligation-induced liver fibrosis.Conclusions: IL-17 induces liver fibrosis through multiple mechanisms in mice. Reagents that block these pathways might be developed as therapeutics for patients with cirrhosis. Mouse Model Immune Response Bone Marrow-Derived Macrophages Myofibroblast Wang, Kai verfasserin aut Aoyama, Tomonori verfasserin aut Grivennikov, Sergei I. verfasserin aut Paik, YongHan verfasserin aut Scholten, David verfasserin aut Cong, Min verfasserin aut Iwaisako, Keiko verfasserin aut Liu, Xiao verfasserin aut Zhang, Mingjun verfasserin aut Österreicher, Christoph H. verfasserin aut Stickel, Felix verfasserin aut Ley, Klaus verfasserin aut Brenner, David A. verfasserin aut Kisseleva, Tatiana verfasserin aut Enthalten in Gastroenterology Stanford, Calif. : HighWire Press, 1965 143 Online-Ressource (DE-627)270937293 (DE-600)1478699-0 (DE-576)078590221 1528-0012 nnns volume:143 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.87 Gastroenterologie AR 143 |
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10.1053/j.gastro.2012.05.049 doi (DE-627)ELV002120313 (ELSEVIER)S0016-5085(12)00817-7 DE-627 ger DE-627 rda eng 610 DE-600 44.87 bkl Meng, Fanli verfasserin aut Interleukin-17 Signaling in Inflammatory, Kupffer Cells, and Hepatic Stellate Cells Exacerbates Liver Fibrosis in Mice 2012 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background & Aims: Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.Methods: Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis in wild-type mice with that of IL-17RA −/− mice and of bone marrow chimeric mice devoid of IL-17 signaling in immune and Kupffer cells (IL-17RA −/− to wild-type and IL-17A −/− to wild-type mice) or liver resident cells (wild-type to IL-17RA −/− mice).Results: In response to liver injury, levels of Il-17A and its receptor increased. IL-17A increased appeared to promote fibrosis by activating inflammatory and liver resident cells. IL-17 signaling facilitated production of IL-6, IL-1, and tumor necrosis factor-α by inflammatory cells and increased the expression of transforming growth factor-1, a fibrogenic cytokine. IL-17 directly induced production of collagen type I in hepatic stellate cells by activating the signal transducer and activator of transcription 3 (Stat3) signaling pathway. Mice devoid of Stat3 signaling in hepatic stellate cells (GFAPStat3 −/− mice) were less susceptible to fibrosis. Furthermore, deletion of IL-23 from immune cells attenuated liver fibrosis, whereas deletion of IL-22 exacerbated fibrosis. Administration of IL-22 and IL-17E (IL-25, a negative regulator of IL-23) protected mice from bile duct ligation-induced liver fibrosis.Conclusions: IL-17 induces liver fibrosis through multiple mechanisms in mice. Reagents that block these pathways might be developed as therapeutics for patients with cirrhosis. Mouse Model Immune Response Bone Marrow-Derived Macrophages Myofibroblast Wang, Kai verfasserin aut Aoyama, Tomonori verfasserin aut Grivennikov, Sergei I. verfasserin aut Paik, YongHan verfasserin aut Scholten, David verfasserin aut Cong, Min verfasserin aut Iwaisako, Keiko verfasserin aut Liu, Xiao verfasserin aut Zhang, Mingjun verfasserin aut Österreicher, Christoph H. verfasserin aut Stickel, Felix verfasserin aut Ley, Klaus verfasserin aut Brenner, David A. verfasserin aut Kisseleva, Tatiana verfasserin aut Enthalten in Gastroenterology Stanford, Calif. : HighWire Press, 1965 143 Online-Ressource (DE-627)270937293 (DE-600)1478699-0 (DE-576)078590221 1528-0012 nnns volume:143 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.87 Gastroenterologie AR 143 |
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interleukin-17 signaling in inflammatory, kupffer cells, and hepatic stellate cells exacerbates liver fibrosis in mice |
| title_auth |
Interleukin-17 Signaling in Inflammatory, Kupffer Cells, and Hepatic Stellate Cells Exacerbates Liver Fibrosis in Mice |
| abstract |
Background & Aims: Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.Methods: Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis in wild-type mice with that of IL-17RA −/− mice and of bone marrow chimeric mice devoid of IL-17 signaling in immune and Kupffer cells (IL-17RA −/− to wild-type and IL-17A −/− to wild-type mice) or liver resident cells (wild-type to IL-17RA −/− mice).Results: In response to liver injury, levels of Il-17A and its receptor increased. IL-17A increased appeared to promote fibrosis by activating inflammatory and liver resident cells. IL-17 signaling facilitated production of IL-6, IL-1, and tumor necrosis factor-α by inflammatory cells and increased the expression of transforming growth factor-1, a fibrogenic cytokine. IL-17 directly induced production of collagen type I in hepatic stellate cells by activating the signal transducer and activator of transcription 3 (Stat3) signaling pathway. Mice devoid of Stat3 signaling in hepatic stellate cells (GFAPStat3 −/− mice) were less susceptible to fibrosis. Furthermore, deletion of IL-23 from immune cells attenuated liver fibrosis, whereas deletion of IL-22 exacerbated fibrosis. Administration of IL-22 and IL-17E (IL-25, a negative regulator of IL-23) protected mice from bile duct ligation-induced liver fibrosis.Conclusions: IL-17 induces liver fibrosis through multiple mechanisms in mice. Reagents that block these pathways might be developed as therapeutics for patients with cirrhosis. |
| abstractGer |
Background & Aims: Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.Methods: Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis in wild-type mice with that of IL-17RA −/− mice and of bone marrow chimeric mice devoid of IL-17 signaling in immune and Kupffer cells (IL-17RA −/− to wild-type and IL-17A −/− to wild-type mice) or liver resident cells (wild-type to IL-17RA −/− mice).Results: In response to liver injury, levels of Il-17A and its receptor increased. IL-17A increased appeared to promote fibrosis by activating inflammatory and liver resident cells. IL-17 signaling facilitated production of IL-6, IL-1, and tumor necrosis factor-α by inflammatory cells and increased the expression of transforming growth factor-1, a fibrogenic cytokine. IL-17 directly induced production of collagen type I in hepatic stellate cells by activating the signal transducer and activator of transcription 3 (Stat3) signaling pathway. Mice devoid of Stat3 signaling in hepatic stellate cells (GFAPStat3 −/− mice) were less susceptible to fibrosis. Furthermore, deletion of IL-23 from immune cells attenuated liver fibrosis, whereas deletion of IL-22 exacerbated fibrosis. Administration of IL-22 and IL-17E (IL-25, a negative regulator of IL-23) protected mice from bile duct ligation-induced liver fibrosis.Conclusions: IL-17 induces liver fibrosis through multiple mechanisms in mice. Reagents that block these pathways might be developed as therapeutics for patients with cirrhosis. |
| abstract_unstemmed |
Background & Aims: Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.Methods: Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis in wild-type mice with that of IL-17RA −/− mice and of bone marrow chimeric mice devoid of IL-17 signaling in immune and Kupffer cells (IL-17RA −/− to wild-type and IL-17A −/− to wild-type mice) or liver resident cells (wild-type to IL-17RA −/− mice).Results: In response to liver injury, levels of Il-17A and its receptor increased. IL-17A increased appeared to promote fibrosis by activating inflammatory and liver resident cells. IL-17 signaling facilitated production of IL-6, IL-1, and tumor necrosis factor-α by inflammatory cells and increased the expression of transforming growth factor-1, a fibrogenic cytokine. IL-17 directly induced production of collagen type I in hepatic stellate cells by activating the signal transducer and activator of transcription 3 (Stat3) signaling pathway. Mice devoid of Stat3 signaling in hepatic stellate cells (GFAPStat3 −/− mice) were less susceptible to fibrosis. Furthermore, deletion of IL-23 from immune cells attenuated liver fibrosis, whereas deletion of IL-22 exacerbated fibrosis. Administration of IL-22 and IL-17E (IL-25, a negative regulator of IL-23) protected mice from bile duct ligation-induced liver fibrosis.Conclusions: IL-17 induces liver fibrosis through multiple mechanisms in mice. Reagents that block these pathways might be developed as therapeutics for patients with cirrhosis. |
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| title_short |
Interleukin-17 Signaling in Inflammatory, Kupffer Cells, and Hepatic Stellate Cells Exacerbates Liver Fibrosis in Mice |
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Wang, Kai Aoyama, Tomonori Grivennikov, Sergei I. Paik, YongHan Scholten, David Cong, Min Iwaisako, Keiko Liu, Xiao Zhang, Mingjun Österreicher, Christoph H. Stickel, Felix Ley, Klaus Brenner, David A. Kisseleva, Tatiana |
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Wang, Kai Aoyama, Tomonori Grivennikov, Sergei I. Paik, YongHan Scholten, David Cong, Min Iwaisako, Keiko Liu, Xiao Zhang, Mingjun Österreicher, Christoph H. Stickel, Felix Ley, Klaus Brenner, David A. Kisseleva, Tatiana |
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| doi_str |
10.1053/j.gastro.2012.05.049 |
| up_date |
2024-07-06T23:41:01.234Z |
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