Advances in the pathogenesis and relationship between intestinal flora and inflammatory bowel disease

doi:10.3877/cma.j.issn.2095-7157.2022.03.007

Abstract

Abstract:

Inflammatory bowel disease (IBD) is a type of chronic and recurrent inflammatory bowel disease, the exact etiology of which is unknown. IBD is mainly characterized by intestinal inflammation caused by abnormal immune response. Genetic susceptibility genes and environmental factors such as diet, smoking, and antibiotic use are the main causes of its pathogenesis. A large number of studies have revealed the important role of gut microbiota in maintaining intestinal homeostasis. Intestinal microbiota dysbiosis not only affects host metabolism, but also leads to intestinal immune dysregulation in hosts with genetically susceptible genes, thereby inducing intestinal inflammation. This article reviewed the pathogenesis of inflammatory bowel disease and its relationship with the gut microbiota.

Key words: Inflammatory bowel disease, Genetic gene, Gut barrier, Immune regulatory mechanism, Gut microbiota

Quanlong Yang, Chongxi Fan, Xuehui Shi, Mengnan Xu, Tao Sun, Shoubin Ning. Advances in the pathogenesis and relationship between intestinal flora and inflammatory bowel disease[J]. Chinese Journal of Gastrointestinal Endoscopy(Electronic Edition), 2022, 09(03): 148-151.

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References 37

[1]	卞冬生．炎症性肠病中的营养不良与少肌症[J]．肠外与肠内营养，2018, 25(1): 56-61.
[2]	李学锋，彭霞，周明欢．我国炎症性肠病流行病学研究进展[J]．现代消化及介入诊疗，2020, 25(9): 1265-1267.
[3]	Jostins L, Ripke S, Weersma RK，et al.Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease[J]. Nature, 2012, 491(7422): 119-124.
[4]	Ananthakrishnan AN, Luo C, Yajnik V，et al.Gut Microbiome Function Predicts Response to Anti-integrin Biologic Therapy in Inflammatory Bowel Diseases[J]．Cell Host Microbe，2017，21(5): 603-610.
[5]	Sokol H, Brot L, Stefanescu C，et al.Prominence of ileal mucosa-associated microbiota to predict postoperative endoscopic recurrence in Crohn′s disease[J]．Gut，2020，69(3): 462-472.
[6]	Tan G, Zeng B, Zhi FC.Regulation of human enteric alpha-defensins by NOD2 in the Paneth cell lineage[J]．Eur J Cell Biol，2015，94(1): 60-66.
[7]	Yilmaz B, Juillerat P, Oyas O，et al.Publisher Correction：Microbial network disturbances in relapsing refractory Crohn′s disease[J]．Natur Med，2019，25(4): 701-701.
[8]	Hampe J, Franke A, Rosenstiel P，et al.A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1[J]. Natur Gene, 2007, 39(2): 207-211.
[9]	Drummond RA, Franco LM, Lionakis MS.Human CARD9：A Critical Molecule of Fungal Immune Surveillance[J]．Front Immunol，2018，9: 1836-1842.
[10]	Jhingran A, Kasahara S, Shepardson KM，et al.Compartment-specific and sequential role of MyD88 and CARD9 in chemokine induction and innate defense during respiratory fungal infection[J]．PloS Pathog, 2015, 11(1): e1004589.
[11]	Yang E, Shen J．The roles and functions of Paneth cells in Crohn′s disease: A critical review[J]．Cell Prolif，2021，54(1): e12958.
[12]	Liu Z, Lee J, Krummey S，et al.The kinase LRRK2 is a regulator of the transcription factor NFAT that modulates the severity of inflammatory bowel disease[J]．Natur Immunol，2011，12(11):1063-1070.
[13]	Adolph TE, Tomczak MF, Niederreiter L，et al.Paneth cells as a site of origin for intestinal inflammation[J]．Nature，2013，503(7475):272-276.
[14]	Valatas V, Kolios G, Bamias G．TL1A (TNFSF15) and DR3 (TNFRSF25): A Co-stimulatory System of Cytokines With Diverse Functions in Gut Mucosal Immunity[J]．Front Immunol，2019，10: 583-596.
[15]	Yamamoto H, Nakamura Y, Sato K，et al.Defect of CARD9 leads to impaired accumulation of gamma interferon-producing memory phenotype T cells in lungs and increased susceptibility to pulmonary infection with Cryptococcus neoformans[J]．Infect Immun，2014, 82(4): 1606-1615.
[16]	Sokol H, Conway KL, Zhang M，et al.Card9 mediates intestinal epithelial cell restitution, T-helper 17 responses, and control of bacterial infection in mice[J]．Gastroenterology，2013，145(3): 591-601,e593.
[17]	刘志昌，余稳稳，周海存，等．与炎症性肠病相关的环境因素的研究进展[J]．中华炎性肠病杂志，2021，5(4): 360-363.
[18]	Peloquin JM, Goel G, Villablanca EJ，et al.Mechanisms of Pediatric Inflammatory Bowel Disease[J]．Ann Rev Immunol，2016，34(1): 31-64.
[19]	Morton H, Pedley KC, Stewart RJC，et al.Inflammatory Bowel Disease：Are Symptoms and Diet Linked？[J]．Nutrients，2020，12(10):2957-2970.
[20]	杨佳，于君．饮食、肠道微生态与结直肠癌[J/CD]．中华结直肠疾病电子杂志，2019, 8(6): 541-545.
[21]	Chen L, Wang J, Yi J，et al.Increased mucin-degrading bacteria by high protein diet leads to thinner mucus layer and aggravates experimental colitis[J]．J Gastroenterol Hepatol，2021，36(10):2864-2874.
[22]	曾胜澜，张荣臻，王娜，等．饮食-肠道菌群轴对非酒精性脂肪性肝病的影响[J]．临床肝胆病杂志，2021, 37(11): 2676-2679.
[23]	杨礼丹，何訸，安振梅．肠道菌群在代谢相关脂肪性肝病中的作用[J]．临床肝胆病杂志，2021, 37(9): 2231-2235.
[24]	Laffin M, Fedorak R, Zalasky A，et al.A high-sugar diet rapidly enhances susceptibility to colitis via depletion of luminal short-chain fatty acids in mice[J]．Sci Rep，2019, 9(1): 12294-12304.
[25]	Johansson ME, Phillipson M, Petersson J，et al.The inner of the two Muc2 mucin-dependent mucus layers in colon is devoid of bacteria[J]. Proc Natl Acad Sci USA，2008，105(39): 15064-15069.
[26]	Shan M, Gentile M, Yeiser JR，et al.Mucus enhances gut homeostasis and oral tolerance by delivering immunoregulatory signals[J]．Science, 2013, 342(6157): 447-453.
[27]	徐鹏飞，周千惠，廖雨晗，等．易感基因-潘氏细胞-肠道微生态轴在炎症性肠病中的作用[J]．中华炎性肠病杂志，2022, 6(1): 83-86.
[28]	Ye Y, Yosuke S, Noam J，et al.1097-Tl1A Overexpression Drives Paneth Cell Hyperplasia and Prevents Maturation of Lysozyme Containing Granules in the Presence of Intact Microbiota[J]. Gastroenterology，2018, 154(6): S216.
[29]	Rivas MA, Beaudoin M, Gardet A，et al.Deep resequencing of GWAS loci identifies independent rare variants associated with inflammatory bowel disease[J]．Natur Gene，2011，43(11): 1066-1073.
[30]	Dong Y, Fan C, Hu W，et al.Melatonin attenuated early brain injury induced by subarachnoid hemorrhage via regulating NLRP3 inflammasome and apoptosis signaling[J]．J Pineal Res，2016，60(3): 253-262.
[31]	Mazmanian SK, Liu CH, Tzianabos AO，et al.An immunomodulatory molecule of symbiotic bacteria directs maturation of the host immune system[J]．Cell，2005，122(1):107-118.
[32]	董雯迪，张海蓉，李瑞，等．调节性T淋巴细胞/辅助性T淋巴细胞17在自身免疫性肝炎发生发展中的作用机制及其相关治疗靶点[J]. 临床肝胆病杂志，2021, 37(10): 2456-2460.
[33]	Alroqi FJ, Chatila TA.T Regulatory Cell Biology in Health and Disease[J]．Curr Allergy Asthma Rep, 2016，16(4): 27-34.
[34]	Fantini MC, Rizzo A, Fina D，et al.Smad7 controls resistance of colitogenic T cells to regulatory T cell-mediated suppression[J]. Gastroenterology，2009，136(4): 1308-1316.
[35]	Franke A, Balschun T, Karlsen TH，et al.Sequence variants in IL10, ARPC2 and multiple other loci contribute to ulcerative colitis susceptibility[J]．Natur Genet，2008，40(11):1319-1323.
[36]	Hoshi N, Schenten D, Nish SA，et al.MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice[J]. Natur Commun，2012，3:1120-1129.
[37]	Roy U, Galvez EJC, Iljazovic A，et al.Distinct microbial communities trigger colitis development upon intestinal barrier damage via innate or adaptive immune cells[J]．Cell Rep，2017，21(4): 994-1008.

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