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It is becoming increasingly clear that the ‘one microbe-one disease’ paradigm must be reconsidered, because it fails to account for the pathogenesis of several common human illnesses with ever-increasing socioeconomic impacts (such as IBD). Notably, instability within the gut's microbial communities (referred to as dysbiosis) has been linked to loss of gut barrier function in IBD. In particular, IBDs are associated with a greater preponderance of certain Bacteroidetes and a lower abundance of Firmicutes.1 ,2 Likewise, several targeted approaches in mice have revealed that the major Crohn's disease-predisposing NOD2 gene has a role in protecting against intestinal inflammation afforded by some Bacteroides spp (including B vulgatus).3 ,4 Remarkably, reciprocal transplantation of faecal microbiota from Nod2-deficient mice enhanced the vulnerability of control animals to colonic injury.3 In line with reverse genetic studies in mice, subclinical dysbiosis has been observed in healthy, first-degree relatives of patients with Crohn's disease.5 One can therefore reasonably presume that familial similarities in the microbiome are related to similar host genetic compositions.3 ,6 Consistently, twin studies have demonstrated that variations in the host genome may influence the structure and composition of the …
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