Inflammatory bowel disease (IBD) is characterised by dysregulated chronic inflammation throughout the intestinal tract with unknown causes. Aetiology of IBD is speculated to be the result of a complex interplay among genetic predisposition, dysregulated immune response, gut microbiome and environmental factors. Despite the identification of various risk genes, a substantial impact of genetic risk on our understanding of the pathogenesis of IBD remains limited. In addition, a complete understanding of the functional significance of IBD risk loci remains for the most part unknown. In Gut , a series of elegant in vivo experiments performed by Hazime et al provided new insight into the functional significance of dual oxidase 2 (DUOX2) signalling in promoting colitis using genetically engineered vTLR4 mice. 1 Notably, Hazime et al demonstrated that DUOX2 leads to gut barrier dysfunction and microbial alteration. Using vTLR4 mice as a model of epithelial-specific DUOX2 overactivation and vTLR4 DUOXA IEC-KO...
Inflammatory bowel disease (IBD) is characterised by dysregulated chronic inflammation throughout the intestinal tract with unknown causes. Aetiology of IBD is speculated to be the result of a complex interplay among genetic predisposition, dysregulated immune response, gut microbiome and environmental factors. Despite the identification of various risk genes, a substantial impact of genetic risk on our understanding of the pathogenesis of IBD remains limited. In addition, a complete understanding of the functional significance of IBD risk loci remains for the most part unknown. In Gut , a series of elegant in vivo experiments performed by Hazime et al provided new insight into the functional significance of dual oxidase 2 (DUOX2) signalling in promoting colitis using genetically engineered vTLR4 mice. 1 Notably, Hazime et al demonstrated that DUOX2 leads to gut barrier dysfunction and microbial alteration. Using vTLR4 mice as a model of epithelial-specific DUOX2 overactivation and vTLR4 DUOXA IEC-KO...