PLoS ONE (Jan 2016)

Association of Ulcerative Colitis with FUT2 and FUT3 Polymorphisms in Patients from Southeast China.

  • Dingyuan Hu,
  • Daguan Zhang,
  • Shuzi Zheng,
  • Maodong Guo,
  • Xinxin Lin,
  • Yi Jiang

DOI
https://doi.org/10.1371/journal.pone.0146557
Journal volume & issue
Vol. 11, no. 1
p. e0146557

Abstract

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Dysbiosis of intestinal microbiota has been implicated in ulcerative colitis (UC). Fucosyltransferase (FUT) 2 and FUT3 determine expression of histo-blood group antigens in the gut and may affect the intestinal microbiota. We investigated the association between FUT2 and FUT3 polymorphisms and UC in Chinese patients.We genotyped FUT2 (rs281377, rs1047781 and rs601338) and FUT3 (rs28362459, rs3745635 and rs3894326) in 485 UC patients and 580 healthy controls using SNaPshot. We also evaluated expression of Lewis a and b antigens in the sigmoid colon of 7 UC patients and 7 patients with benign colonic polyps.The frequencies of mutant allele (A) and genotype (GA+AA) in FUT3 (rs3745635) were higher in UC patients than controls (P = 0.016, 95%CI: 1.339-1.699; P = 0.038, 95%CI: 1.330-1.742, respectively). Stratified analyses revealed that the frequencies of mutant allele (G) and genotype (TG+GG) of FUT3 (rs28362459) were significantly lower in patients with extensive colitis than those with distal colitis (P<0.001, 95%CI: 0.503-0.742; P = 0.001, 95%CI: 0.567-0.786, respectively). Similar conclusions were drawn for the mutant allele (A) and genotype (GA+AA) of FUT3 (rs3745635) in patients with extensive colitis compared to those with distal colitis (P = 0.006, 95%CI: 0.553-0.845; P = 0.011, 95%CI: 0.621-0.900, respectively). Although expression of Lewis b antigen in the sigmoid colon did not differ between UC patients and controls, Lewis a antigen expression was higher in the cryptic epithelium of both inflammatory and non-inflammatory sigmoid colon of UC patients than controls (P = 0.028).Our findings indicated that polymorphisms in FUT3 and its intestinal expression might be associated with UC pathogenesis.