IL6 genetic variants haplotype is associated with susceptibility and disease activity but not with therapy response in p
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ORIGINAL ARTICLE
IL6 genetic variants haplotype is associated with susceptibility and disease activity but not with therapy response in patients with inflammatory bowel disease Beatriz Piantoni Gonçalves 1,2 & Tamires Flauzino 1 & Cláudia Junko Inoue 1,2 & Jaqueline Costa Castardo de Paula 1 & Talita Cristina Galvão 1 & Camila Cataldi de Alcantara 1 & Paula Kikuchi Miyazaki 1 & Lucilene Rosa & Silva Westmore 2 & Marcell Alysson Batisti Lozovoy 3 & Edna Maria Vissoci Reiche 3 & Andréa Name Colado Simão 3 Accepted: 8 September 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Purpose The aim of the present study was to evaluate the IL6 −174 G>C (rs1800795) and −572 G>C (rs1800796) genetic variants and their association with inflammatory bowel diseases (IBDs), disease activity, and response to TNF-α inhibitors. Methods The study included 178 patients with IBD and 224 healthy controls. Among the IBD patients, 66 of them were in use of TNF-α inhibitors therapy and were followed during 48 weeks and categorized as responders and non-responders. Results In total, 89 (50.0%) had ulcerative colitis (UC) and 89 (50.0%) had Crohn’s disease (CD). The IL6 −572 CC genotype presented a protective effect in CD patients in codominant and recessive models, while the IL6 −174 CC genotype was associated with susceptibility to UC and CD. The presence of G/C haplotype in the recessive model (GCGC) was associated with UC. The Crohn’s disease endoscopic index of severity was low in those patients carrying the GCGC haplotype. It was observed that there was no association between the IL6 genetic variants and TNF-α inhibitor therapy response. Conclusion The G/C haplotype (recessive model) was associated with susceptibility to UC but not to CD. However, the G/C haplotype (dominant model) was associated with the endoscopic activity of CD. Moreover, these IL6 variants did not predict the TNF-α inhibitor therapy response. Keywords Inflammatory bowel diseases, Ulcerative colitis, Crohn’s disease, interleukin 6 genetic variant, rs1800796, rs1800795
Introduction Inflammatory bowel diseases (IBDs) are heterogeneous chronic inflammatory disorders of the gastrointestinal tract resulting from an abnormal immune response against the normal microbiota. The incidence and prevalence of IBD are dramatically increasing worldwide [1], and its etiology is * Andréa Name Colado Simão [email protected] 1
Laboratory of Research in Applied Immunology, State University of Londrina, Londrina, PR, Brazil
2
Outpatient Clinic of Gastroenterology, University Hospital, State University of Londrina, Londrina, PR, Brazil
3
Department of Pathology, Clinical Analysis and Toxicology, Health Sciences Center, University Hospital, State University of Londrina, Av. Robert Koch 60, Londrina, PR 86038-440, Brazil
multifactorial with a complex interaction between genetic variants, immune response of the host, and environmental factors [2, 3]. The two major examples of IBD are ulcerative colitis (UC) and Crohn’s disease (CD); while CD has long been
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