肠道微生态与自发性细菌性腹膜炎的关系

刘玉; 张宇一; 邹颖; 袁伟; 郭红英; 梅雪; 王介非; 钱志平

doi:10.3969/j.issn.1001-5256.2021.02.037

肠道微生态与自发性细菌性腹膜炎的关系

DOI: 10.3969/j.issn.1001-5256.2021.02.037

上海市公共卫生临床中心重症肝病科，上海 201508

基金项目:

国家“十二五”科技重大专项 (2018ZX10725506-002);

2018年院级科研课题 (KY-GW-2018-23)

作者贡献声明:刘玉、张宇一、邹颖负责课题设计，资料分析，撰写论文；袁伟、郭红英、梅雪参与收集数据，修改论文；王介非、钱志平负责拟定写作思路，指导撰写文章并最后定稿。

详细信息

作者简介:
刘玉(1984—)，女，主治医师，主要从事病毒学肝炎等肝病临床研究

通信作者:
钱志平，qianzhiping@shphc.org.cn

中图分类号: R575.2
计量
- 文章访问数: 591
- HTML全文浏览量: 83
- PDF下载量: 60
- 被引次数: 0
出版历程
- 收稿日期: 2020-08-05
- 录用日期: 2020-09-24
- 出版日期: 2021-02-20

Association between intestinal microecology and spontaneous bacterial peritonitis

Department of Severe Liver Disease, Shanghai Public Health Clinical Center, Shanghai 201508, China

摘要

摘要: 自发性细菌性腹膜炎(SBP)是终末期肝病的常见严重并发症，肠道微生态与SBP的发生、发展及预后密切相关，细菌易位是SBP发病的关键机制。归纳了肝硬化患者的肠道微生态特征，简述了肠道菌群在SBP发生、进展中的作用机制，为临床调整肠道微生态改善SBP提供理论基础。
- 腹膜炎 /
- 肝硬化 /
- 胃肠道微生物组 /
- 感染
Abstract: Spontaneous bacterial peritonitis (SBP) is a common serious complication of end-stage liver disease. Intestinal microecology is closely associated with the development, progression, and prognosis of SBP, and bacterial translocation is the key pathogenesis of SBP. This article summarizes the intestinal microecology in patients with liver cirrhosis and briefly describes the mechanism of action of intestinal flora in the development and progression of SBP, thus providing a theoretical basis for the clinical regulation of intestinal microecology and treatment of SBP.
- Peritonitis /
- Liver Cirrhosis /
- Gastrointestinal Microbiome /
- Infection

HTML全文

参考文献(43)

[1]	FIORE M, MARAOLO AE, GENTILE I, et al. Current concepts and future strategies in the antimicrobial therapy of emerging Gram-positive spontaneous bacterial peritonitis[J]. World J Hepatol, 2017, 9(30): 1166-1175. DOI: 10.4254/wjh.v9.i30.1166
[2]	SHIZUMA T. Spontaneous bacterial and fungal peritonitis in patients with liver cirrhosis: A literature review[J]. World J Hepatol, 2018, 10(2): 254-266. DOI: 10.4254/wjh.v10.i2.254
[3]	FLOCH MH. Intestinal microecology in health and wellness[J]. J Clin Gastroenterol, 2011, 10: s108-s110.
[4]	WU ZW, LI LJ. Bacterial infection of liver cirrhosis and intestinal flora[J]. J Mod Med Health, 2019, 35(2): 161-163. (in Chinese) DOI: 10.3969/j.issn.1009-5519.2019.02.001 吴仲文, 李兰娟. 肝硬化细菌感染与肠道菌群[J]. 现代医药卫生, 2019, 35(2): 161-163. DOI: 10.3969/j.issn.1009-5519.2019.02.001
[5]	D'ARGENIO V, SALVATORE F. The role of the gut microbiome in the healthy adult status[J]. Clin Chim Acta, 2015, 451(Pt A): 97-102.
[6]	SMITH K. Liver disease: Kupffer cells regulate the progression of ALD and NAFLD[J]. Nat Rev Gastroenterol Hepatol, 2013, 10(9): 503.
[7]	PETRASEK J, BALA S, CSAK T, et al. IL-1 receptor antagonist ameliorates inflammasome-dependent alcoholic steatohepatitis in mice[J]. J Clin Invest, 2012, 122(10): 3476-3489. DOI: 10.1172/JCI60777
[8]	OLEFSKY JM, GLASS CK. Macrophages, inflammation, and insulin resistance[J]. Annu Rev Physiol, 2010, 72: 219-246. DOI: 10.1146/annurev-physiol-021909-135846
[9]	TILG H, CANI PD, MAYER EA. Gut microbiome and liver diseases[J]. Gut, 2016, 65(12): 2035-2044. DOI: 10.1136/gutjnl-2016-312729
[10]	MILOSEVIC I, VUJOVIC A, BARAC A, et al. Gut-liver axis, gut microbiota, and its modulation in the management of liver diseases: A review of the literature[J]. Int J Mol Sci, 2019, 20(2): 395. DOI: 10.3390/ijms20020395
[11]	REUTER B, BAJAJ JS. Microbiome: Emerging concepts in patients with chronic liver disease[J]. Clin Liver Dis, 2020, 24(3): 493-520. DOI: 10.1016/j.cld.2020.04.006
[12]	SCHULTALBERS M, TERGAST TL, SIMON N, et al. Frequency, characteristics and impact of multiple consecutive nosocomial infections in patients with decompensated liver cirrhosis and ascites[J]. United European Gastroenterol J, 2020, 8(5): 567-576. DOI: 10.1177/2050640620913732
[13]	OLSON JC, WENDON JA, KRAMER DJ, et al. Intensive care of the patient with cirrhosis[J]. Hepatology, 2011, 54(5): 1864-1872. DOI: 10.1002/hep.24622
[14]	SEKI E, SCHNABL B. Role of innate immunity and the microbiota in liver fibrosis: Crosstalk between the liver and gut[J]. J Physiol, 2012, 590(3): 447-458. DOI: 10.1113/jphysiol.2011.219691
[15]	de ROZA MA, KAI L, KAM JW, et al. Proton pump inhibitor use increases mortality and hepatic decompensation in liver cirrhosis[J]. World J Gastroenterol, 2019, 25: 4933-4944. DOI: 10.3748/wjg.v25.i33.4933
[16]	QIN N, YANG F, LI A, et al. Alterations of the human gut microbiome in liver cirrhosis[J]. Nature, 2014, 513(7516): 59-64. DOI: 10.1038/nature13568
[17]	BAJAJ JS, BETRAPALLY NS, GILLEVET PM. Decompensated cirrhosis and microbiome interpretation[J]. Nature, 2015, 525(7569): e1-e2. DOI: 10.1038/nature14851
[18]	WANG Y, PAN CQ, XING H. Advances in gut microbiota of viral hepatitis cirrhosis[J]. Biomed Res Int, 2019, 2019: 9726786.
[19]	USAMI M, MIYOSHI M, YAMASHITA H. Gut microbiota and host metabolism in liver cirrhosis[J]. World J Gastroenterol, 2015, 21(41): 11597-11608. DOI: 10.3748/wjg.v21.i41.11597
[20]	BAJAJ JS, BETRAPALLY NS, HYLEMON PB, et al. Salivary microbiota reflects changes in gut microbiota in cirrhosis with hepatic encephalopathy[J]. Hepatology, 2015, 62(4): 1260-1271. DOI: 10.1002/hep.27819
[21]	LUAN YT, CAI WJ, JIANG SL, et al. A comparative study of intestinal flora between hepatitis B cirrhosis patients with or without ascites[J]. J Clin Hepatol, 2020, 36(7): 1520-1526. (in Chinese) DOI: 10.3969/j.issn.1001-5256.2020.07.015 栾雨婷, 蔡文君, 蒋轼丽, 等. 乙型肝炎肝硬化患者伴或不伴腹水对肠道菌群的影响[J]. 临床肝胆病杂志, 2020, 36(7): 1520-1526. DOI: 10.3969/j.issn.1001-5256.2020.07.015
[22]	WIEST R, KRAG A, GERBES A. Spontaneous bacterial peritonitis: Recent guidelines and beyond[J]. Gut, 2012, 61(2): 297-310. DOI: 10.1136/gutjnl-2011-300779
[23]	HADJIVASILIS A, TZANIS A, IOAKIM KJ, et al. The diagnostic accuracy of ascitic calprotectin for the early diagnosis of spontaneous bacterial peritonitis: Systematic review and meta-analysis[J]. Eur J Gastroenterol Hepatol, 2021, 33(3): 312-318.
[24]	GUNDLING F, SCHMIDTLER F, HAPFELMEIER A, et al. Fecal calprotectin is a useful screening parameter for hepatic encephalopathy and spontaneous bacterial peritonitis in cirrhosis[J]. Liver Int, 2011, 31(9): 1406-1415. DOI: 10.1111/j.1478-3231.2011.02577.x
[25]	WEIL D, HEURGUE-BERLOT A, MONNET E, et al. Accuracy of calprotectin using the Quantum Blue Reader for the diagnosis of spontaneous bacterial peritonitis in liver cirrhosis[J]. Hepatol Res, 2019, 49(1): 72-81. DOI: 10.1111/hepr.13239
[26]	JUNG Y, WEN T, MINGLER MK, et al. IL-1β in eosinophil-mediated small intestinal homeostasis and IgA production[J]. Mucosal Immunol, 2015, 8(4): 930-942. DOI: 10.1038/mi.2014.123
[27]	LV XY, DING HG, ZHENG JF, et al. Rifaximin improves survival in cirrhotic patients with refractory ascites: A real-world study[J]. World J Gastroenterol, 2020, 26(2): 199-218. DOI: 10.3748/wjg.v26.i2.199
[28]	ASSIMAKOPOULOS SF, TSAMANDAS AC, TSIAOUSSIS GI, et al. Altered intestinal tight junctions' expression in patients with liver cirrhosis: A pathogenetic mechanism of intestinal hyperpermeability[J]. Eur J Clin Invest, 2012, 42(4): 439-446. DOI: 10.1111/j.1365-2362.2011.02609.x
[29]	RAWAT M, NIGHOT M, AL-SADI R, et al. IL1B increases intestinal tight junction permeability by upregulation of MIR200C-3p, which degrades occludin mRNA[J]. Gastroenterology, 2020, 159(4): 1375-1389. DOI: 10.1053/j.gastro.2020.06.038
[30]	SCARPELLINI E, VALENZA V, GABRIELLI M, et al. Intestinal permeability in cirrhotic patients with and without spontaneous bacterial peritonitis: Is the ring closed?[J]. Am J Gastroenterol, 2010, 105(2): 323-327. DOI: 10.1038/ajg.2009.558
[31]	MUÑOZ L, JOSÉ BORRERO M, UBEDA M, et al. Interaction between intestinal dendritic cells and bacteria translocated from the gut in rats with cirrhosis[J]. Hepatology, 2012, 56(5): 1861-1869. DOI: 10.1002/hep.25854
[32]	APPENRODT B, GRVNHAGE F, GENTEMANN MG, et al. Nucleotide-binding oligomerization domain containing 2 (NOD2) variants are genetic risk factors for death and spontaneous bacterial peritonitis in liver cirrhosis[J]. Hepatology, 2010, 51(4): 1327-1333. DOI: 10.1002/hep.23440
[33]	NISCHALKE HD, BERGER C, ALDENHOFF K, et al. Toll-like receptor (TLR) 2 promoter and intron 2 polymorphisms are associated with increased risk for spontaneous bacterial peritonitis in liver cirrhosis[J]. J Hepatol, 2011, 55(5): 1010-1016. DOI: 10.1016/j.jhep.2011.02.022
[34]	BRUNS T, PETER J, REUKEN PA, et al. NOD2 gene variants are a risk factor for culture-positive spontaneous bacterial peritonitis and monomicrobial bacterascites in cirrhosis[J]. Liver Int, 2012, 32(2): 223-230. DOI: 10.1111/j.1478-3231.2011.02561.x
[35]	HOLLMAN DA, MILONA A, van ERPECUM KJ, et al. Anti-inflammatory and metabolic actions of FXR: Insights into molecular mechanisms[J]. Biochim Biophys Acta, 2012, 1821(11): 1443-1452. DOI: 10.1016/j.bbalip.2012.07.004
[36]	LUTZ P, BERGER C, LANGHANS B, et al. A farnesoid X receptor polymorphism predisposes to spontaneous bacterial peritonitis[J]. Dig Liver Dis, 2014, 46(11): 1047-1050. DOI: 10.1016/j.dld.2014.07.008
[37]	STEIB CJ, SCHEWE J, GERBES AL. Infection as a trigger for portal hypertension[J]. Dig Dis, 2015, 33(4): 570-576. DOI: 10.1159/000375352
[38]	QUAN M, XING HC. Research progress on intestinal flora and chronic liver diseases[J/CD]. Chin J Liver Dis (Electronic Version), 2019, 11(3): 26-30. (in Chinese) 全敏, 邢卉春. 肠道菌群与慢性肝病相关研究进展[J/CD]. 中国肝脏病杂志(电子版), 2019, 11(3): 26-30.
[39]	HORVATH A, DURDEVIC M, LEBER B, et al. Changes in the intestinal microbiome during a multispecies probiotic intervention in compensated cirrhosis[J]. Nutrients, 2020, 12(6): e1874. DOI: 10.3390/nu12061874
[40]	HORVATH A, LEBER B, SCHMERBOECK B, et al. Randomised clinical trial: The effects of a multispecies probiotic vs. placebo on innate immune function, bacterial translocation and gut permeability in patients with cirrhosis[J]. Aliment Pharmacol Ther, 2016, 44(9): 926-935. DOI: 10.1111/apt.13788
[41]	DENG X, ZHENG C, WANG S, et al. Treatment with a probiotic combination reduces abdominal adhesion in rats by decreasing intestinal inflammation and restoring microbial composition[J]. Oncol Rep, 2020, 43(3): 986-998.
[42]	HⅡPPALA K, JOUHTEN H, RONKAINEN A, et al. The potential of gut commensals in reinforcing intestinal barrier function and alleviating inflammation[J]. Nutrients, 2018, 10(8): 988. DOI: 10.3390/nu10080988
[43]	MITTAL H, WYAWAHARE M, SISTLA S. Microbiological profile of pathogens in spontaneous bacterial peritonitis secondary to liver cirrhosis: A retrospective study[J]. Trop Doct, 2020, 50(2): 138-141. DOI: 10.1177/0049475520905745