131
Views
0
CrossRef citations to date
0
Altmetric
ORIGINAL RESEARCH

Identification of Targets for Subsequent Treatment of Crohn’s Disease Patients After Failure of Anti-TNF Therapy

, , , , & ORCID Icon
Pages 4617-4631 | Received 25 May 2023, Accepted 20 Sep 2023, Published online: 17 Oct 2023

References

  • Roda G, Chien Ng S, Kotze PG, et al. Crohn’s disease. Nat Rev Dis Primers. 2020;6(1):22. doi:10.1038/s41572-020-0156-2
  • Lamb CA, Kennedy NA, Raine T, et al. British society of gastroenterology consensus guidelines on the management of inflammatory bowel disease in adults. Gut. 2019;68(Suppl 3):s1–s106. doi:10.1136/gutjnl-2019-318484
  • Peyrin-Biroulet L, Fiorino G, Buisson A, Danese S. First-line therapy in adult Crohn’s disease: who should receive anti-TNF agents? Nat Rev Gastroenterol Hepatol. 2013;10(6):345–351. doi:10.1038/nrgastro.2013.31
  • Cohen BL, Sachar DB. Update on anti-tumor necrosis factor agents and other new drugs for inflammatory bowel disease. BMJ. 2017;357:j2505. doi:10.1136/bmj.j2505
  • C RGM, Chaparro M, Mesonero F, et al. Effectiveness of anti-TNFalpha drugs in patients with Crohn’s disease who do not achieve remission with their first anti-TNFalpha agent. Dig Liver Dis. 2016;48(6):613–619. doi:10.1016/j.dld.2016.02.012
  • Gisbert JP, Chaparro M. Primary failure to an anti-tnf agent in inflammatory bowel disease: switch (to a Second Anti-TNF Agent) or Swap (for another mechanism of action)? J Clin Med. 2021;10(22):5318. doi:10.3390/jcm10225318
  • Liefferinckx C, Minsart C, Cremer A, et al. Early vedolizumab trough levels at induction in inflammatory bowel disease patients with treatment failure during maintenance. Eur J Gastroenterol Hepatol. 2019;31(4):478–485. doi:10.1097/MEG.0000000000001356
  • Sands BE, Feagan BG, Rutgeerts P, et al. Effects of vedolizumab induction therapy for patients with Crohn’s disease in whom tumor necrosis factor antagonist treatment failed. Gastroenterology. 2014;147(3):618–627 e613. doi:10.1053/j.gastro.2014.05.008
  • Yanai H, Hanauer SB. Assessing response and loss of response to biological therapies in IBD. Am J Gastroenterol. 2011;106(4):685–698. doi:10.1038/ajg.2011.103
  • Davis S, Meltzer PS. GEOquery: a bridge between the Gene Expression Omnibus (GEO) and bioConductor. Bioinformatics. 2007;23(14):1846–1847. doi:10.1093/bioinformatics/btm254
  • Ritchie ME, Phipson B, Wu D, et al. limma powers differential expression analyses for RNA-sequencing and microarray studies. Nucleic Acids Res. 2015;43(7):e47. doi:10.1093/nar/gkv007
  • Kolde R, Laur S, Adler P, Vilo J. Robust rank aggregation for gene list integration and meta-analysis. Bioinformatics. 2012;28(4):573–580. doi:10.1093/bioinformatics/btr709
  • Langfelder P, Horvath S. WGCNA: an R package for weighted correlation network analysis. BMC Bioinform. 2008;9:559. doi:10.1186/1471-2105-9-559
  • The Gene Ontology C. The gene ontology resource: 20 years and still GOing strong. Nucleic Acids Res. 2019;47(D1):D330–D338. doi:10.1093/nar/gky1055
  • Kanehisa M, Furumichi M, Tanabe M, Sato Y, Morishima K. KEGG: new perspectives on genomes, pathways, diseases and drugs. Nucleic Acids Res. 2017;45(D1):D353–D361. doi:10.1093/nar/gkw1092
  • Yu G, Wang LG, Han Y, He QY. clusterProfiler: an R package for comparing biological themes among gene clusters. Omics. 2012;16(5):284–287. doi:10.1089/omi.2011.0118
  • Szklarczyk D, Gable AL, Lyon D, et al. STRING v11: protein-protein association networks with increased coverage, supporting functional discovery in genome-wide experimental datasets. Nucleic Acids Res. 2019;47(D1):D607–d613. doi:10.1093/nar/gky1131
  • Shannon P, Markiel A, Ozier O, et al. Cytoscape: a software environment for integrated models of biomolecular interaction networks. Genome Res. 2003;13(11):2498–2504. doi:10.1101/gr.1239303
  • Chin CH, Chen SH, Wu HH, Ho CW, Ko MT, Lin CY. cytoHubba: identifying hub objects and sub-networks from complex interactome. BMC Syst Biol. 2014;8(4):S11. doi:10.1186/1752-0509-8-S4-S11
  • Gorelik Y, Freilich S, Gerassy-Vainberg S, et al. Antibiotic use differentially affects the risk of anti-drug antibody formation during anti-TNFalpha therapy in inflammatory bowel disease patients: a report from the epi-IIRN. Gut. 2022;71(2):287–295. doi:10.1136/gutjnl-2021-325185
  • Reichel CA, Puhr-Westerheide D, Zuchtriegel G, et al. C-C motif chemokine CCL3 and canonical neutrophil attractants promote neutrophil extravasation through common and distinct mechanisms. Blood. 2012;120(4):880–890. doi:10.1182/blood-2012-01-402164
  • Hughes CE, Nibbs RJB. A guide to chemokines and their receptors. Febs j. 2018;285(16):2944–2971. doi:10.1111/febs.14466
  • Ramos CD, Canetti C, Souto JT, et al. MIP-1alpha[CCL3] acting on the CCR1 receptor mediates neutrophil migration in immune inflammation via sequential release of TNF-alpha and LTB4. J Leukoc Biol. 2005;78(1):167–177. doi:10.1189/jlb.0404237
  • Banks C, Bateman A, Payne R, Johnson P, Sheron N. Chemokine expression in IBD. Mucosal chemokine expression is unselectively increased in both ulcerative colitis and Crohn’s disease. J Pathol. 2003;199(1):28–35. doi:10.1002/path.1245
  • Boro M, Balaji KN. CXCL1 and CXCL2 Regulate NLRP3 Inflammasome Activation via G-Protein-Coupled Receptor CXCR2. J Immunol. 2017;199(5):1660–1671. doi:10.4049/jimmunol.1700129
  • De Filippo K, Dudeck A, Hasenberg M, et al. Mast cell and macrophage chemokines CXCL1/CXCL2 control the early stage of neutrophil recruitment during tissue inflammation. Blood. 2013;121(24):4930–4937. doi:10.1182/blood-2013-02-486217
  • Sawant KV, Sepuru KM, Lowry E, et al. Neutrophil recruitment by chemokines Cxcl1/KC and Cxcl2/MIP2: role of Cxcr2 activation and glycosaminoglycan interactions. J Leukoc Biol. 2021;109(4):777–791. doi:10.1002/JLB.3A0820-207R
  • Arijs I, De Hertogh G, Machiels K, et al. Mucosal gene expression of cell adhesion molecules, chemokines, and chemokine receptors in patients with inflammatory bowel disease before and after infliximab treatment. Am J Gastroenterol. 2011;106(4):748–761. doi:10.1038/ajg.2011.27
  • Cripps JG, Celaj S, Burdick M, Strieter RM, Gorham JD. Liver inflammation in a mouse model of Th1 hepatitis despite the absence of invariant NKT cells or the Th1 chemokine receptors CXCR3 and CCR5. Lab Invest. 2012;92(10):1461–1471. doi:10.1038/labinvest.2012.104
  • Sandborn WJ, Rutgeerts P, Colombel JF, et al. Eldelumab [anti-interferon-gamma-inducible protein-10 antibody] induction therapy for active crohn’s disease: a randomised, double-blind, placebo-controlled phase iia study. J Crohns Colitis. 2017;11(7):811–819. doi:10.1093/ecco-jcc/jjx005
  • Friedrich M, Pohin M, Powrie F. Cytokine networks in the pathophysiology of inflammatory bowel disease. Immunity. 2019;50(4):992–1006. doi:10.1016/j.immuni.2019.03.017
  • Bank S, Julsgaard M, Abed OK, et al. Polymorphisms in the NFkB, TNF-alpha, IL-1beta, and IL-18 pathways are associated with response to anti-TNF therapy in Danish patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2019;49(7):890–903. doi:10.1111/apt.15187
  • Bank S, Andersen PS, Burisch J, et al. Associations between functional polymorphisms in the NFkappaB signaling pathway and response to anti-TNF treatment in Danish patients with inflammatory bowel disease. Pharmacogenomics J. 2014;14(6):526–534. doi:10.1038/tpj.2014.19
  • Martin JC, Chang C, Boschetti G, et al. Single-cell analysis of Crohn’s disease lesions identifies a pathogenic cellular module associated with resistance to Anti-TNF therapy. Cell. 2019;178(6):1493–1508 e1420. doi:10.1016/j.cell.2019.08.008
  • Devlin JC, Axelrad J, Hine AM, et al. Single-cell transcriptional survey of ileal-anal pouch immune cells from ulcerative colitis patients. Gastroenterology. 2021;160(5):1679–1693. doi:10.1053/j.gastro.2020.12.030
  • Dosh RH, Jordan-Mahy N, Sammon C, Le Maitre C. Interleukin 1 is a key driver of inflammatory bowel disease-demonstration in a murine IL-1Ra knockout model. Oncotarget. 2019;10(37):3559–3575. doi:10.18632/oncotarget.26894
  • Soderman J, Berglind L, Almer S. Gene expression-genotype analysis implicates GSDMA, GSDMB, and LRRC3C as Contributors to inflammatory bowel disease susceptibility. Biomed Res Int. 2015;2015:834805. doi:10.1155/2015/834805
  • Shi YJ, Hu SJ, Zhao QQ, Liu XS, Liu C, Wang H. Toll-like receptor 4 (TLR4) deficiency aggravates dextran sulfate sodium (DSS)-induced intestinal injury by down-regulating IL6, CCL2 and CSF3. Ann Transl Med. 2019;7(23):713. doi:10.21037/atm.2019.12.28
  • Prins MM, Verstockt B, Ferrante M, Vermeire S, Wildenberg ME, Koelink PJ. Monocyte TREM-1 levels associate with anti-TNF Responsiveness in IBD through autophagy and fcgamma-receptor signaling pathways. Front Immunol. 2021;12:627535. doi:10.3389/fimmu.2021.627535
  • Caer C, Gorreja F, Forsskahl SK, et al. TREM-1+ macrophages define a pathogenic cell subset in the intestine of Crohn’s disease patients. J Crohns Colitis. 2021;15(8):1346–1361. doi:10.1093/ecco-jcc/jjab022
  • Danese S, Vermeire S, Hellstern P, et al. Randomised trial and open-label extension study of an anti-interleukin-6 antibody in Crohn’s disease (ANDANTE I and II). Gut. 2019;68(1):40–48. doi:10.1136/gutjnl-2017-314562
  • Leal RF, Planell N, Kajekar R, et al. Identification of inflammatory mediators in patients with Crohn’s disease unresponsive to anti-TNFalpha therapy. Gut. 2015;64(2):233–242. doi:10.1136/gutjnl-2013-306518
  • Dahlqvist J, Fulco CP, Ray JP, et al. Systematic identification of genomic elements that regulate FCGR2A expression and harbor variants linked with autoimmune disease. Hum Mol Genet. 2022;31(12):1946–1961. doi:10.1093/hmg/ddab372
  • Castro-Dopico T, Dennison TW, Ferdinand JR, et al. Anti-commensal IgG drives intestinal inflammation and type 17 immunity in ulcerative colitis. Immunity. 2019;50(4):1099–1114 e1010. doi:10.1016/j.immuni.2019.02.006