AI Article Synopsis

  • Inflammatory bowel disease (IBD) is heavily influenced by inflammation, with oxidative stress playing a significant role in its development and connection to cancer.
  • The intestinal mucosa's antioxidant system is impaired in IBD, which may be linked to genetic variants in antioxidant genes, potentially increasing susceptibility to Crohn's disease (CD) and ulcerative colitis (UC).
  • A study of a Portuguese population identified a specific genetic variant in the GPX1 gene that is significantly associated with ulcerative colitis, while associations found with the SOD2 gene and Crohn's disease were not statistically strong enough after further analysis.

Article Abstract

Inflammation is the driving force in inflammatory bowel disease (IBD) and its link to oxidative stress and carcinogenesis has long been accepted. The antioxidant system of the intestinal mucosa in IBD is compromised resulting in increased oxidative injury. This defective antioxidant system may be the result of genetic variants in antioxidant genes, which can represent susceptibility factors for IBD, namely Crohn's disease (CD) and ulcerative colitis (UC). Single nucleotide polymorphisms (SNPs) in the antioxidant genes SOD2 (rs4880) and GPX1 (rs1050450) were genotyped in a Portuguese population comprising 436 Crohn's disease and 367 ulcerative colitis patients, and 434 healthy controls. We found that the AA genotype in GPX1 is associated with ulcerative colitis (OR = 1.93, adjusted P-value = 0.037). Moreover, we found nominal significant associations between SOD2 and Crohn's disease susceptibility and disease subphenotypes but these did not withstand the correction for multiple testing. These findings indicate a possible link between disease phenotypes and antioxidant genes. These results suggest a potential role for antioxidant genes in IBD pathogenesis and should be considered in future association studies.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5215755PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0169102PLOS

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