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巨噬细胞在原发性胆汁性胆管炎发病中的作用机制及影响

马狄 邰文琳

引用本文:
Citation:

巨噬细胞在原发性胆汁性胆管炎发病中的作用机制及影响

DOI: 10.12449/JCH240126
基金项目: 

国家自然科学基金 (82060385);

昆明医科大学2023年研究生创新基金 (2023S321)

利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:马狄负责收集资料及文章撰写;邰文琳负责文章修改及定稿。
详细信息
    通信作者:

    邰文琳, taiwenlin2685@163.com (ORCID: 0000-0002-8278-929X)

The role and impact of macrophages in the pathogenesis of primary biliary cholangitis

Research funding: 

National Natural Science Foundation of China (82060385);

The Postgraduate Innovation Fund Project of Kunming Medical University 2023 (2023S321)

More Information
  • 摘要: 原发性胆汁性胆管炎(PBC)是一种以肝内胆汁淤积为特征表现的慢性自身免疫性疾病,免疫因素导致进行性小胆管破坏,胆汁淤积,最终发展为肝纤维化、肝硬化甚至肝衰竭。巨噬细胞作为一群具有功能异质性的群体,在PBC整个疾病进程中发挥着不同的作用。本文归纳了巨噬细胞参与PBC发病机制的可能方式,讨论了其对PBC的影响及相关潜在治疗靶点。本文指出巨噬细胞主要参与了PBC损伤中的先天性免疫,且与肠道微生物失调相联系,在疾病后期与胆汁淤积、肝纤维化、肝硬化有关。

     

  • [1] GULAMHUSEIN AF, HIRSCHFIELD GM. Primary biliary cholangitis: Pathogenesis and therapeutic opportunities[J]. Nat Rev Gastroenterol Hepatol, 2020, 17( 2): 93- 110. DOI: 10.1038/s41575-019-0226-7.
    [2] LLEO A, WANG GQ, GERSHWIN ME, et al. Primary biliary cholangitis[J]. Lancet, 2020, 396( 10266): 1915- 1926. DOI: 10.1016/S0140-6736(20)31607-X.
    [3] COLAPIETRO F, BERTAZZONI A, LLEO A. Contemporary epidemiology of primary biliary cholangitis[J]. Clin Liver Dis, 2022, 26( 4): 555- 570. DOI: 10.1016/j.cld.2022.06.001.
    [4] LI H, GUAN YL, HAN CC, et al. The pathogenesis, models and therapeutic advances of primary biliary cholangitis[J]. Biomed Pharmacother, 2021, 140: 111754. DOI: 10.1016/j.biopha.2021.111754.
    [5] WU Y, FAN XX, YU HC, et al. Macrophage polarization is involved in liver fibrosis induced by β1-adrenoceptor autoantibody[J]. Acta Biochim Biophys Sin, 2022, 54( 8): 1100- 1112. DOI: 10.3724/abbs.2022102.
    [6] HEYMANN F, TACKE F. Immunology in the liver: From homeostasis to disease[J]. Nat Rev Gastroenterol Hepatol, 2016, 13( 2): 88- 110. DOI: 10.1038/nrgastro.2015.200.
    [7] RONCA V, MANCUSO C, MILANI C, et al. Immune system and cholangiocytes: A puzzling affair in primary biliary cholangitis[J]. J Leukoc Biol, 2020, 108( 2): 659- 671. DOI: 10.1002/JLB.5MR0320-200R.
    [8] LLEO A, LEUNG PSC, HIRSCHFIELD GM, et al. The pathogenesis of primary biliary cholangitis: A comprehensive review[J]. Semin Liver Dis, 2020, 40( 1): 34- 48. DOI: 10.1055/s-0039-1697617.
    [9] MA WT, CHEN DK. Immunological abnormalities in patients with primary biliary cholangitis[J]. Clin Sci, 2019, 133( 6): 741- 760. DOI: 10.1042/CS20181123.
    [10] SHAO T, LEUNG PSC, ZHANG W, et al. Treatment with a JAK1/2 inhibitor ameliorates murine autoimmune cholangitis induced by IFN overexpression[J]. Cell Mol Immunol, 2022, 19( 10): 1130- 1140. DOI: 10.1038/s41423-022-00904-y.
    [11] TIAN XB, WANG Y, LU Y, et al. Conditional depletion of macrophages ameliorates cholestatic liver injury and fibrosis via lncRNA-H19[J]. Cell Death Dis, 2021, 12( 7): 646. DOI: 10.1038/s41419-021-03931-1.
    [12] ZHANG XM, THOMPKINS-JOHNS A, ZIOBER A, et al. Hepatic macrophage types cluster with disease etiology in chronic liver disease and differ compared to normal liver: Implications for their biologic and diagnostic role[J]. Int J Surg Pathol, 2023, 31( 3): 268- 279. DOI: 10.1177/10668969221099630.
    [13] BRUNEAU A, GUILLOT A, TACKE F. Macrophages in cholangiopathies[J]. Curr Opin Gastroenterol, 2022, 38( 2): 114- 120. DOI: 10.1097/MOG.0000000000000814.
    [14] FU HY, BAO WM, YANG CX, et al. Kupffer cells regulate natural killer cells via the NK group 2, member D(NKG2D)/retinoic acid early inducible-1(RAE-1) interaction and cytokines in a primary biliary cholangitis mouse model[J]. Med Sci Monit, 2020, 26: e923726. DOI: 10.12659/MSM.923726.
    [15] LI X, LIU RP, WANG YY, et al. Cholangiocyte-derived exosomal lncRNA H19 promotes macrophage activation and hepatic inflammation under cholestatic conditions[J]. Cells, 2020, 9( 1): 190. DOI: 10.3390/cells9010190.
    [16] YANG Y, CHOI J, CHEN Y, et al. E. coli and the etiology of human PBC: Antimitochondrial antibodies and spreading determinants[J]. Hepatology, 2022, 75( 2): 266- 279. DOI: 10.1002/hep.32172.
    [17] REUVENI D, GORE Y, LEUNG PSC, et al. The critical role of chemokine(C-C motif) receptor 2-positive monocytes in autoimmune cholangitis[J]. Front Immunol, 2018, 9: 1852. DOI: 10.3389/fimmu.2018.01852.
    [18] CHEN RL, TANG RQ, MA X, et al. Immunologic responses and the pathophysiology of primary biliary cholangitis[J]. Clin Liver Dis, 2022, 26( 4): 583- 611. DOI: 10.1016/j.cld.2022.06.003.
    [19] DUKIĆ M, RADONJIĆ T, JOVANOVIĆ I, et al. Alcohol, inflammation, and microbiota in alcoholic liver disease[J]. Int J Mol Sci, 2023, 24( 4): 3735. DOI: 10.3390/ijms24043735.
    [20] CADAMURO M, GIRARDI N, GORES GJ, et al. The emerging role of macrophages in chronic cholangiopathies featuring biliary fibrosis: An attractive therapeutic target for orphan diseases[J]. Front Med, 2020, 7: 115. DOI: 10.3389/fmed.2020.00115.
    [21] PINTO C, GIORDANO DM, MARONI L, et al. Role of inflammation and proinflammatory cytokines in cholangiocyte pathophysiology[J]. Biochim Biophys Acta Mol Basis Dis, 2018, 1864( 4 Pt B): 1270- 1278. DOI: 10.1016/j.bbadis.2017.07.024.
    [22] TANAKA A. Current understanding of primary biliary cholangitis[J]. Clin Mol Hepatol, 2021, 27( 1): 1- 21. DOI: 10.3350/cmh.2020.0028.
    [23] RONCA V, CHEN QB, LYGOURA V, et al. Autoantibodies in patients with interleukin 12 receptor beta 1 deficiency[J]. J Dig Dis, 2019, 20( 7): 363- 370. DOI: 10.1111/1751-2980.12790.
    [24] MAYO MJ. Mechanisms and molecules: What are the treatment targets for primary biliary cholangitis?[J]. Hepatology, 2022, 76( 2): 518- 531. DOI: 10.1002/hep.32405.
    [25] MU N, LIN F, JIANG ZG, et al. Characteristics of serum chemokine profile in primary biliary cholangitis[J]. Cytokine, 2020, 136: 155291. DOI: 10.1016/j.cyto.2020.155291.
    [26] RAMACHANDRAN P, DOBIE R, WILSON-KANAMORI JR, et al. Resolving the fibrotic niche of human liver cirrhosis at single-cell level[J]. Nature, 2019, 575( 7783): 512- 518. DOI: 10.1038/s41586-019-1631-3.
    [27] BUONOMO EL, MEI SL, GUINN SR, et al. Liver stromal cells restrict macrophage maturation and stromal IL-6 limits the differentiation of cirrhosis-linked macrophages[J]. J Hepatol, 2022, 76( 5): 1127- 1137. DOI: 10.1016/j.jhep.2021.12.036.
    [28] DAEMEN S, GAINULLINA A, KALUGOTLA G, et al. Dynamic shifts in the composition of resident and recruited macrophages influence tissue remodeling in NASH[J]. Cell Rep, 2021, 34( 2): 108626. DOI: 10.1016/j.celrep.2020.108626.
    [29] GUILLOT A, WINKLER M, SILVA AFONSO M, et al. Mapping the hepatic immune landscape identifies monocytic macrophages as key drivers of steatohepatitis and cholangiopathy progression[J]. Hepatology, 2023, 78( 1): 150- 166. DOI: 10.1097/HEP.0000000000000270.
    [30] CAI SY, GE MX, MENNONE A, et al. Inflammasome is activated in the liver of cholestatic patients and aggravates hepatic injury in bile duct-ligated mouse[J]. Cell Mol Gastroenterol Hepatol, 2020, 9( 4): 679- 688. DOI: 10.1016/j.jcmgh.2019.12.008.
    [31] LIAO M, LIAO JW, QU JQ, et al. Hepatic TNFRSF12A promotes bile acid-induced hepatocyte pyroptosis through NFκB/Caspase-1/GSDMD signaling in cholestasis[J]. Cell Death Discov, 2023, 9( 1): 26. DOI: 10.1038/s41420-023-01326-z.
    [32] KODA S, ZHANG BB, ZHOU QY, et al. β2-adrenergic receptor enhances the alternatively activated macrophages and promotes biliary injuries caused by helminth infection[J]. Front Immunol, 2021, 12: 754208. DOI: 10.3389/fimmu.2021.754208.
    [33] GALLUCCI GM, ALSUWAYT B, AUCLAIR AM, et al. Fenofibrate downregulates NF-κB signaling to inhibit pro-inflammatory cytokine secretion in human THP-1 macrophages and during primary biliary cholangitis[J]. Inflammation, 2022, 45( 6): 2570- 2581. DOI: 10.1007/s10753-022-01713-1.
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出版历程
  • 收稿日期:  2023-03-25
  • 录用日期:  2023-04-15
  • 出版日期:  2024-01-23
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