Role of interleukin-22 in the development and progression of liver fibrosis

Yuxi MENG; Lijuan HUO

doi:10.3969/j.issn.1001-5256.2021.12.039

Volume 37 Issue 12

Dec. 2021

Turn off MathJax

Article Contents

Abstract

References

Article Navigation > Journal of Clinical Hepatology > 2021 > 37(12): 2924-2927

PDF( 1878 KB)

Role of interleukin-22 in the development and progression of liver fibrosis

DOI: 10.3969/j.issn.1001-5256.2021.12.039

Yuxi MENG¹,
Lijuan HUO^{2
,
,}

1.
Department of Gastroenterology, The Second Hospital Affiliated to Shanxi Medical University, Taiyuan 030001, China
2.
Department of Gastroenterology, The First Hospital Affiliated to Shanxi Medical University, Taiyuan 030001, China

Received Date: 2021-04-22
Accepted Date: 2021-06-07
Published Date: 2021-12-20

Abstract

Abstract

Liver fibrosis is the result of persistent inflammatory response and chronic scar healing response during chronic liver injury and may progress to liver cirrhosis, portal hypertension, and liver failure, which finally requires liver transplantation. Interleukin-22 (IL-22) belongs to the IL-10 family and is the only cytokine that is produced by immune cells but does not act on immune cells. IL-22 plays a role by binding to its receptors IL-22R1 and IL-10R2, which has attracted much attention in the field of liver disease research in recent years. IL-22 not only plays the role of anti-inflammation and promotion of liver regeneration and tissue repair, but also has a pro-inflammatory effect in liver diseases, and it exerts a protective effect on the liver by reducing fibrosis in some pathological conditions, but there are still controversies over its association with liver fibrosis. IL-22 has different effects and mechanisms in liver fibrosis caused by different etiologies. This article reviews the role and possible mechanisms of IL-22 in liver fibrosis caused by viral infection (HBV and HCV), alcohol, high-fat diet, and autoimmunity.
- Liver Cirrhosis,
- Interleukin-22,
- Pathologic Processes

FullText(HTML)

References(32)

References

[1]	BÖTTCHER K, PINZANI M. Pathophysiology of liver fibrosis and the methodological barriers to the development of anti-fibrogenic agents[J]. Adv Drug Deliv Rev, 2017, 121: 3-8. DOI: 10.1016/j.addr.2017.05.016.
[2]	DUVAL F, MORENO-CUEVAS JE, GONZÁLEZ-GARZA MT, et al. Liver fibrosis and protection mechanisms action of medicinal plants targeting apoptosis of hepatocytes and hepatic stellate cells[J]. Adv Pharmacol Sci, 2014, 2014: 373295. DOI: 10.1155/2014/373295.
[3]	LEE YA, WALLACE MC, FRIEDMAN SL. Pathobiology of liver fibrosis: A translational success story[J]. Gut, 2015, 64(5): 830-841. DOI: 10.1136/gutjnl-2014-306842.
[4]	DUMOUTIER L, LOUAHED J, RENAULD JC. Cloning and characterization of IL-10-related T cell-derived inducible factor (IL-TIF), a novel cytokine structurally related to IL-10 and inducible by IL-9[J]. J Immunol, 2000, 164(4): 1814-1819. DOI: 10.4049/jimmunol.164.4.1814.
[5]	DUDAKOV JA, HANASH AM, van DEN BRINK MR. Interleukin-22: Immunobiology and pathology[J]. Annu Rev Immunol, 2015, 33: 747-785. DOI: 10.1146/annurev-immunol-032414-112123.
[6]	SABAT R, OUYANG W, WOLK K. Therapeutic opportunities of the IL-22-IL-22R1 system[J]. Nat Rev Drug Discov, 2014, 13(1): 21-38. DOI: 10.1038/nrd4176.
[7]	GAO B, XIANG X. Interleukin-22 from bench to bedside: A promising drug for epithelial repair[J]. Cell Mol Immunol, 2019, 16(7): 666-667. DOI: 10.1038/s41423-018-0055-6.
[8]	WOLK K, WITTE E, WITTE K, et al. Biology of interleukin-22[J]. Semin Immunopathol, 2010, 32(1): 17-31. DOI: 10.1007/s00281-009-0188-x.
[9]	PARK O, WANG H, WENG H, et al. In vivo consequences of liver-specific interleukin-22 expression in mice: Implications for human liver disease progression[J]. Hepatology, 2011, 54(1): 252-261. DOI: 10.1002/hep.24339.
[10]	XIANG X, GUI H, KING NJ, et al. IL-22 and non-ELR-CXC chemokine expression in chronic hepatitis B virus-infected liver[J]. Immunol Cell Biol, 2012, 90(6): 611-619. DOI: 10.1038/icb.2011.79.
[11]	FENG D, KONG X, WENG H, et al. Interleukin-22 promotes proliferation of liver stem/progenitor cells in mice and patients with chronic hepatitis B virus infection[J]. Gastroenterology, 2012, 143(1): 188-198. e7. DOI: 10.1053/j.gastro.2012.03.044.
[12]	ZHAO J, ZHANG Z, LUAN Y, et al. Pathological functions of interleukin-22 in chronic liver inflammation and fibrosis with hepatitis B virus infection by promoting T helper 17 cell recruitment[J]. Hepatology, 2014, 59(4): 1331-1342. DOI: 10.1002/hep.26916.
[13]	ROLLA S, ALCHERA E, IMARISIO C, et al. The balance between IL-17 and IL-22 produced by liver-infiltrating T-helper cells critically controls NASH development in mice[J]. Clin Sci (Lond), 2016, 130(3): 193-203. DOI: 10.1042/CS20150405.
[14]	WU LY, LIU S, LIU Y, et al. Up-regulation of interleukin-22 mediates liver fibrosis via activating hepatic stellate cells in patients with hepatitis C[J]. Clin Immunol, 2015, 158(1): 77-87. DOI: 10.1016/j.clim.2015.03.003.
[15]	SERTORIO M, HOU X, CARMO RF, et al. IL-22 and IL-22 binding protein (IL-22BP) regulate fibrosis and cirrhosis in hepatitis C virus and schistosome infections[J]. Hepatology, 2015, 61(4): 1321-1331. DOI: 10.1002/hep.27629.
[16]	BATALLER R, GAO B. Liver fibrosis in alcoholic liver disease[J]. Semin Liver Dis, 2015, 35(2): 146-156. DOI: 10.1055/s-0035-1550054.
[17]	KI SH, PARK O, ZHENG M, et al. Interleukin-22 treatment ameliorates alcoholic liver injury in a murine model of chronic-binge ethanol feeding: Role of signal transducer and activator of transcription 3[J]. Hepatology, 2010, 52(4): 1291-1300. DOI: 10.1002/hep.23837.
[18]	HENDRIKX T, DUAN Y, WANG Y, et al. Bacteria engineered to produce IL-22 in intestine induce expression of REG3G to reduce ethanol-induced liver disease in mice[J]. Gut, 2019, 68(8): 1504-1515. DOI: 10.1136/gutjnl-2018-317232.
[19]	NI YH, HUO LJ, LI TT. Antioxidant axis Nrf2-keap1-ARE in inhibition of alcoholic liver fibrosis by IL-22[J]. World J Gastroenterol, 2017, 23(11): 2002-2011. DOI: 10.3748/wjg.v23.i11.2002.
[20]	CHALASANI N, YOUNOSSI Z, LAVINE JE, et al. The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases[J]. Hepatology, 2018, 67(1): 328-357. DOI: 10.1002/hep.29367.
[21]	WANG X, OTA N, MANZANILLO P, et al. Interleukin-22 alleviates metabolic disorders and restores mucosal immunity in diabetes[J]. Nature, 2014, 514(7521): 237-241. DOI: 10.1038/nature13564.
[22]	CHEN Z, DOWNING S, TZANAKAKIS ES. Four decades after the discovery of regenerating islet-derived (Reg) proteins: Current understanding and challenges[J]. Front Cell Dev Biol, 2019, 7: 235. DOI: 10.3389/fcell.2019.00235.
[23]	ZAI W, CHEN W, WU Z, et al. Targeted interleukin-22 gene delivery in the liver by polymetformin and penetratin-based hybrid nanoparticles to treat nonalcoholic fatty liver disease[J]. ACS Appl Mater Interfaces, 2019, 11(5): 4842-4857. DOI: 10.1021/acsami.8b19717.
[24]	ZHU J, ZHOU M, ZHAO X, et al. Blueberry, combined with probiotics, alleviates non-alcoholic fatty liver disease via IL-22-mediated JAK1/STAT3/BAX signaling[J]. Food Funct, 2018, 9(12): 6298-6306. DOI: 10.1039/c8fo01227j.
[25]	OH JH, SCHUELER KL, STAPLETON DS, et al. Secretion of recombinant interleukin-22 by engineered lactobacillus reuteri reduces fatty liver disease in a mouse model of diet-induced obesity[J]. mSphere, 2020, 5(3): e00183-20. DOI: 10.1128/mSphere.00183-20.
[26]	LI Y, TANG R, MA X. Epigenetics of primary biliary cholangitis[J]. Adv Exp Med Biol, 2020, 1253: 259-283. DOI: 10.1007/978-981-15-3449-2_10.
[27]	KAWATA K, TSUDA M, YANG GX, et al. Identification of potential cytokine pathways for therapeutic intervention in murine primary biliary cirrhosis[J]. PLoS One, 2013, 8(9): e74225. DOI: 10.1371/journal.pone.0074225.
[28]	HSUEH YH, CHANG YN, LOH CE, et al. AAV-IL-22 modifies liver chemokine activity and ameliorates portal inflammation in murine autoimmune cholangitis[J]. J Autoimmun, 2016, 66: 89-97. DOI: 10.1016/j.jaut.2015.10.005.
[29]	KONG X, FENG D, WANG H, et al. Interleukin-22 induces hepatic stellate cell senescence and restricts liver fibrosis in mice[J]. Hepatology, 2012, 56(3): 1150-1159. DOI: 10.1002/hep.25744.
[30]	HU BL, SHI C, LEI RE, et al. Interleukin-22 ameliorates liver fibrosis through miR-200a/beta-catenin[J]. Sci Rep, 2016, 6: 36436. DOI: 10.1038/srep36436.
[31]	MENG F, WANG K, AOYAMA T, et al. Interleukin-17 signaling in inflammatory, Kupffer cells, and hepatic stellate cells exacerbates liver fibrosis in mice[J]. Gastroenterology, 2012, 143(3): 765-776. e3. DOI: 10.1053/j.gastro.2012.05.049.
[32]	CHOI Y, ABDELMEGEED MA, SONG BJ. Diet high in fructose promotes liver steatosis and hepatocyte apoptosis in C57BL/6J female mice: Role of disturbed lipid homeostasis and increased oxidative stress[J]. Food Chem Toxicol, 2017, 103: 111-121. DOI: 10.1016/j.fct.2017.02.039.

Relative Articles

[1]	Jun GAO, Huan CHEN, Yan LIU, Feng ZHANG, Yuzheng ZHUGE. Effect of interleukin-22 on hepatic stellate cell activation and its mechanism[J]. Journal of Clinical Hepatology, 2024, 40(11): 2229-2237. doi: 10.12449/JCH241116
[2]	Yekai ZONG, Jiangkai LIU. The physiological and pathological role of amyloid protein in the liver[J]. Journal of Clinical Hepatology, 2023, 39(11): 2730-2737. doi: 10.3969/j.issn.1001-5256.2023.11.031
[3]	Feiyan LI, Minggang WANG, Dewen MAO, Xiongbin GUI. Role of gasdermin D in the pathological progression of liver diseases[J]. Journal of Clinical Hepatology, 2023, 39(3): 707-712. doi: 10.3969/j.issn.1001-5256.2023.03.035
[4]	Xiaolu ZHAO, Chunyan ZHANG, Xiaoyang GAO, Yuehong MA. Mechanism of action of the Hippo/YAP pathway in the development and progression of liver fibrosis[J]. Journal of Clinical Hepatology, 2022, 38(7): 1654-1657. doi: 10.3969/j.issn.1001-5256.2022.07.037
[5]	Xin LUO, Ying QU, Xiaobo CAI, Lungen LU. Effects of antiviral therapy on the reversal of liver fibrosis[J]. Journal of Clinical Hepatology, 2022, 38(11): 2596-2598. doi: 10.3969/j.issn.1001-5256.2022.11.032
[6]	Wenzheng YOU, Wanlei REN, Shiying XUAN, Doudou HU. Association between intrahepatic bile duct alterations and liver fibrosis[J]. Journal of Clinical Hepatology, 2022, 38(1): 187-190. doi: 10.3969/j.issn.1001-5256.2022.01.032
[7]	Fan Chang, Wu FuRong, Zhang JiaFu, Jiang Hui. Role of pyroptosis in the pathogenesis of hepatic fibrosis[J]. Journal of Clinical Hepatology, 2020, 36(5): 1138-1140. doi: 10.3969/j.issn.1001-5256.2020.05.042
[8]	YANG Jing, GAO Hong, ZHAO YaoWei, WANG Rui. Role of liver sinusoidal endothelial cells in the pathogenesis of nonalcoholic fatty liver disease[J]. Journal of Clinical Hepatology, 2020, 36(11): 2601-2605. doi: 10.3969/j.issn.1001-5256.2020.11.046
[9]	Geng WenJing, Liu Hui, Ding HuiGuo. Recent advances in drug-induced liver injury: Potential mechanisms, pathological features, and biomarkers[J]. Journal of Clinical Hepatology, 2019, 35(4): 925-929. doi: 10.3969/j.issn.1001-5256.2019.04.049
[10]	Jiang LiNa, Zhao JingMin. A clinical trial on the follow-up of nonalcoholic fatty liver disease: An evaluation of pathological endpoint[J]. Journal of Clinical Hepatology, 2018, 34(12): 2505-2508. doi: 10.3969/j.issn.1001-5256.2018.12.004
[11]	Pan Jing, Pan WenTing, Wu LiHui. Expression and significance of Th22 cells and its functional factor interleukin-22 in mice with autoimmune hepatitis[J]. Journal of Clinical Hepatology, 2018, 34(8): 1745-1749. doi: 10.3969/j.issn.1001-5256.2018.08.030
[12]	Wang BingQiong, Sun YaMeng, You Hong, Shao Chen, Wang TaiLing. Pathological assessment of liver fibrosis regression[J]. Journal of Clinical Hepatology, 2017, 33(3): 435-437. doi: 10.3969/j.issn.1001-5256.2017.03.007
[13]	Bao SuXia, Zheng JianMing, Shi GuangFeng. Research progress in association between interleukin-23 and liver diseases[J]. Journal of Clinical Hepatology, 2016, 32(2): 393-396. doi: 10.3969/j.issn.1001-5256.2016.02.044
[14]	Wang Wei, Zhao RongRong, Yang XiaoFei, Huang ZhangXing, Lian JianQi, Wang JiuPing, Zhang Ye. Influence of Notch signaling pathway on interleukin-22 secreted by CD4~+T cells in patients with hepatitis B[J]. Journal of Clinical Hepatology, 2016, 32(7): 1315-1318. doi: 10.3969/j.issn.1001-5256.2016.07.020
[15]	Wu Qin, Meng FanPing, Ma XueMei, Jin Bo, Shen LiJun, Wu LiBing, Chu JinDong, Lai WenHui, Han JingJing, Li HanWei. Analysis of association between different HCV genotypes and serum interleukin-17, interleukin-6, and vitamin D in patients with HCV-related cirrhosis[J]. Journal of Clinical Hepatology, 2015, 31(11): 1849-1852. doi: 10.3969/j.issn.1001-5256.2015.11.019
[16]	Guan HaiTao, Zhao JinLi, Tang Rui, Sun LinLin. IL-17 promotes expression of fibrosis-related factors in hepatic stellate cells[J]. Journal of Clinical Hepatology, 2013, 29(5): 370-374.
[17]	Wang WeiBin, Zhu YouFu. A brief discussion on pathogenesis of primary biliary cirrhosis[J]. Journal of Clinical Hepatology, 2013, 29(11): 805-809. doi: 10.3969/j.issn.1001-5256.2013.11.002
[18]	Sha XiuJuan, Xin GuiJie, Jin MeiShan, Chi TouMei, Niu JunQi. Pay much attention to the clinical application of pathological examination of liver biopsy in the diagnosis and treatment of liver disease[J]. Journal of Clinical Hepatology, 2012, 28(3): 223-226.

Supplements(0)

Cited By

Cited by

Periodical cited type(4)

1.	宋琳，豆鹏产. 外周血白细胞分化抗原38和IL-22对自身免疫性肝炎患者发生肝硬化的预测效能分析. 国际消化病杂志. 2024(04): 247-250+269 .
2.	于敏，仲跻凤，季瑜. 实时剪切波弹性成像联合血清IL-6/IL-22水平与自身免疫性肝病肝纤维化的相关性. 肝脏. 2024(08): 919-923 .
3.	高君，陈欢，刘燕，张峰，诸葛宇征. 白细胞介素22对肝星状细胞活化的影响及其机制. 临床肝胆病杂志. 2024(11): 2229-2237 . 本站查看
4.	厉姣龙，周振华. 柔肝方对肝纤维化小鼠肝脏内IL-22分泌和IL-22R1表达作用的研究. 上海中医药大学学报. 2022(05): 69-76 .

Other cited types(4)

Proportional views

Proportional views

通讯作者: 陈斌, bchen63@163.com

1.
沈阳化工大学材料科学与工程学院沈阳 110142

Get Citation

PDF

XML

Article Metrics

Article views (781) PDF downloads(55)

Role of interleukin-22 in the development and progression of liver fibrosis

DOI: 10.3969/j.issn.1001-5256.2021.12.039