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

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

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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

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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.

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

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

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