肝巨噬细胞在原发性胆汁性胆管炎发生发展中的作用

杨文霞; 唐映梅

doi:10.3969/j.issn.1001-5256.2020.04.051

肝巨噬细胞在原发性胆汁性胆管炎发生发展中的作用

DOI: 10.3969/j.issn.1001-5256.2020.04.051

昆明医科大学第二附属医院消化内科

基金项目:

国家自然科学基金项目(81360072,8176030241,8166030160)；

详细信息

中图分类号: R575.7
计量
- 文章访问数: 1197
- HTML全文浏览量: 63
- PDF下载量: 198
- 被引次数: 0
出版历程
- 出版日期: 2020-04-20

Role of hepatic macrophages in the development and progression of primary biliary cholangitis

Department of Gastroenterology, The Second Affiliated Hospital of Kunming Medical University

Research funding:

摘要

摘要: 原发性胆汁性胆管炎(PBC)是一种病因未明的以胆汁淤积为特征的慢性自身免疫性肝病,其具体发病机制不明确,其中肝巨噬细胞是PBC免疫和炎症反应及胆管上皮细胞损伤的关键之一;肝巨噬细胞根据来源不同可分为常驻Kupffer细胞和单核细胞来源的巨噬细胞,这些细胞在PBC的发生发展中发挥重要作用。综述了肝巨噬细胞在PBC发生发展中的作用。
- 原发性胆汁性胆管炎 /
- 巨噬细胞 /
- Toll样受体
Abstract: Primary biliary cholangitis( PBC) is a chronic autoimmune liver disease characterized by cholestasis and has unknown etiology.Its specific pathogenesis remains unclear,but hepatic macrophages are one of the key aspects of the immune and inflammatory response of PBC and the injury of biliary epithelial cells. Hepatic macrophages are classified into resident Kupffer cells and monocyte-derived macrophages according to their source,and these cells play an important role in the development and progression of PBC. This article reviews the role of hepatic macrophages in the development and progression of PBC.
- primary biliary cholangitis /
- macrophages /
- Toll-like receptors

HTML全文

参考文献(34)

[1] BEUERS U,GERSHWIN ME,GISH RG,et al. Changing nomenclature for PBC:From ‘cirrhosis’to ‘cholangitis’[J].Hepatology,2015,62(5):1620-1622.

[2] TERZIROLI BERETTA-PICCOLI B,MIELI-VERGANI G,VERGANI D,et al. The challenges of primary biliary cholangitis:What is new and what needs to be done[J]. J Autoimmun,2019,105:102328.

[3] MA WT,CHEN DK. Immunological abnormalities in patients with primary biliary cholangitis[J]. Clin Sci(Lond),2019,133(6):741-760.

[4] RITZ T,KRENKEL O,TACKE F. Dynamic plasticity of macrophage functions in diseased liver[J]. Cell Immunol,2018,330:175-182.

[5] MIHM S. Danger-associated molecular patterns(DAMPs):Molecular triggers for sterile inflammation in the liver[J]. Int J Mol Sci,2018,19(10):3104.

[6] ELCHANINOV AV,FAKTHUDINOV TK,VISHNYAKOVA PA,et al. Phenotypical and functional polymorphism of liver resident macrophages[J]. Cells,2019,8(9):1032.

[7] GUILLOT A,TACKE F. Liver macrophages:Old dogmas and new insights[J]. Hepatol Commun,2019,3(6):730-743.

[8] KOUROUMALIS E,NOTAS G. Primary biliary cirrhosis:From bench to bedside[J]. World J Gastrointest Pharmacol Ther,2015,6(3):32-58.

[9] 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.

[10] PENG A,KE P,ZHAO R,et al. Elevated circulating CD14lowCD16+monocyte subset in primary biliary cirrhosis correlates with liver injury and promotes Th1 polarization[J]. Clin Exp Med,2016,16(4):511-521.

[11] MA WT,GAO F,GU K,et al. The role of monocytes and macrophages in autoimmune diseases:A comprehensive review[J]. Front Immunol,2019,10:1140.

[12] VIOLA A,MUNARI F,SNCHEZ-RODRGUEZ R,et al. The metabolic signature of macrophage responses[J]. Front Immunol,2019,10:1462.

[13] SHAPOURI-MOGHADDAM A,MOHAMMADIAN S,VAZINI H,et al. Macrophage plasticity,polarization,and function in health and disease[J]. J Cell Physiol,2018,233(9):6425-6440.

[14] LIANG Y,QIN BD,SHI H,et al. Analysis for polarization of peripheral monocytes in patients with primary biliary cholangitis[J]. Chin J Clin Lab Sci,2018,36(10):725-728.(in Chinese)梁艳，秦保东，史虹，等．原发性胆汁性胆管炎患者外周血单核细胞极化分析[J]．临床检验杂志，2018,36(10):725-728.

[15] HAN XF. Role of macrophage polarization in primary biliary cirrhosis[D]. Shanghai:Shanghai Jiao Tong University,2011.(in Chinese)韩晓凤．巨噬细胞极化在原发性胆汁性肝硬化中的作用[D]．上海:上海交通大学，2011.

[16] BURSTYN-COHEN T. TAM receptor signaling in development[J]. Int J Dev Biol,2017,61(3-4-5):215-224.

[17] QIN BD. Expression level of TAM receptors signaling pathway in primary biliary cirrhosis and its regulatory mechanism in macrophage polarization[D]. Shanghai:The Second Military Medical University,2016.(in Chinese)秦宝东．TAM信号通路在原发性胆汁性肝硬化患者中的表达水平及其对巨噬细胞极化的影响[D]．上海:第二军医大学，2016.

[18] SUN Q,WANG Q,FENG N,et al. The expression and clinical significance of serum IL-17 in patients with primary biliary cirrhosis[J]. Ann Transl Med,2019,7(16):389.

[19] KENNEDY L,FRANCIS H,INEVRNIZZI P,et al. Secretin/secretin receptor signaling mediates biliary damage and liver fibrosis in early-stage primary biliary cholangitis[J]. FASEB J,2019,33(9):10269-10279.

[20] YE QL,MAO DW,WANG MG,et al. Role of NLRP3 inflammasome in the development and progression of liver diseases[J]. J Clin Hepatol,2019,35(10):2346-2350.(in Chinese)叶倩伶，毛德文，王明刚，等．NOD样受体蛋白3炎性体在肝脏疾病发生发展中的作用[J]．临床肝胆病杂志，2019,35(10):2346-2350.

[21] XIANG GY,FAN J,YE ZY,et al. Expression of NLRP3 inflammasome body and its upstream activator GSDMD in primary biliary cirrhosis[J]. Int J Lab Med,2019,40(17):2049-2057.(in Chinese)向国艳，樊佳，叶震璇，等．NLRP3炎性小体及其上游激活蛋白GSDMD在原发性胆汁性肝硬化中的表达[J]．国际检验医学杂志，2019,40(17):2049-2057.

[22] ARSENIJEVIC A,MILOVANOVIC J,STOJANOVIC B,et al.Gal-3 deficiency suppresses novosphyngobium aromaticivorans inflammasome activation and IL-17 driven autoimmune cholangitis in mice[J]. Front Immunol,2019,10:1309.

[23] TIAN J,YANG G,CHEN HY,et al. Galectin-3 regulates inflammasome activation in cholestatic liver injury[J]. FASEB J,2016,30(12):4202-4213.

[24] GONG Z,ZHOU J,ZHAO S,et al. Chenodeoxycholic acid activates NLRP3 inflammasome and contributes to cholestatic liver fibrosis[J]. Oncotarget,2016,7(51):83951-83963.

[25] GUO C,XIE S,CHI Z,et al. Bile acids control inflammation and metabolic disorder through inhibition of NLRP3 inflammasome[J]. Immunity,2016,45(4):802-816.

[26] DEUTSCHMANN K,REICH M,KLINDT C,et al. Bile acid receptors in the biliary tree:TGR5 in physiology and disease[J]. Biochim Biophys Acta Mol Basis Dis,2018,1864(4 Pt B):1319-1325.

[27] KLINDT C,REICH M,HELLWIG B,et al. The G protein-coupled bile acid receptor TGR5(Gpbar1)modulates endothelin-1 signaling in liver[J]. Cells,2019,8(11):1467.

[28] KEITEL V,STINDT J,HUSSINGER D. Bile acid-activated receptors:GPBAR1(TGR5)and other G protein-coupled receptors[J]. Handb Exp Pharmacol,2019,256:19-49.

[29] PATRA MC,CHOI S. Recent progress in the development of Toll-like receptor(TLR)antagonists[J]. Expert Opin Ther Pat,2016,26(6):719-730.

[30] ZHAO J,ZHAO S,ZHOU G,et al. Altered biliary epithelial cell and monocyte responses to lipopolysaccharide as a TLR ligand in patients with primary biliary cirrhosis[J]. Scand J Gastroenterol,2011,46(4):485-494.

[31] YANG ZX. Study on the requirement of TLR4 for effects of mitochondrial M2 in Pathogenesis of primary biliary cirrhosis[D].Shanghai:The Second Military Medical University,2008.(in Chinese)杨再兴．TLR4介导线粒体M2蛋白致原发性胆汁性肝硬化发病的作用机制研究[D]．上海:第二军医大学，2008.

[32] YU Y,LI MP,XU B,et al. A study of regulatory effects of TLR4 and NF-κB on primary biliary cholangitis[J]. Eur Rev Med Pharmacol Sci,2019,23(9):3951-3959.

[33] MAO TK,LIAN ZX,SELMI C,et al. Altered monocyte responses to defined TLR ligands in patients with primary biliary cirrhosis[J]. Hepatology,2005,42(4):802-808.

[34] SHIMODA S,HARADA K,NIIRO H,et al. Interaction between Toll-like receptors and natural killer cells in the destruction of bile ducts in primary biliary cirrhosis[J]. Hepatology,2011,53(4):1270-1281.

施引文献

资源附件(0)

访问统计