All of the CD patients had established disease and had previously undergone intestinal resection surgery and re-anastamosis; however, interestingly, 45.2% of them were on no treatment at study inclusion. The control group captured patients with a personal or family history of adenomatous colorectal polyps

or cancer in whom the GSK 3 inhibitor right colon had been reached at colonoscopy. Those with infectious colitis, irritable bowel syndrome or occult bleeding were excluded from the study. A nested Helicobacter PCR was positive in 43.8% (24.7% enterohepatic Helicobacter) of the CD cohort and 46.7% (17.4% enterohepatic Helicobacter) of the controls. Once the groups had been adjusted for age, however, there was a significant association between the presence of enterohepatic Helicobacter and CD (OR=2.58, 95% CI 1.04–6.67). Attempts to culture the organisms proved negative. Curiously, PCR for bacterial DNA with universal 16S probes was positive in only 67% of biopsies. It is not clear whether PCR in the CD cohort and control cohort were similarly affected. Sequencing was matched to just two enterohepatic Helicobacter spp., namely

H. pullorum and H. canadensis. A final interesting observation comes from Azevedo et al. (2008) who have shown that Helicobacter spp. including H. felis, H. canadensis, H. pullorum, H. canis, H. mustelae and H. muridarum can survive in water at 25 °C for up Maraviroc concentration to 48 h depending on the species. We have next already discussed the potential for zoonotic and foodborne transmission within this article. This study raises the possibility of waterborne transmission as another route of transmissions. No one has cultured a Helicobacter species from human IBD tissue for use in disease-modelling experiments, and the molecular evidence presented thus far from humans is a veritable patchwork of prevalence figures

and species associations. Our own work outlining the variance between molecular methodologies may explain some of the heterogeneity in prevalence figures, but the variety of species being identified is perhaps harder to reconcile. The closest we have come to attributing human colitic disease to Helicobacter spp. is in the case of H. cinaedi and H. fennelliae and their association with proctitis in homosexual males (see Table 1). The observational and experimental animal data supporting the putative role of Helicobacter spp. in IBD offer strong support, however, to the possibility that these agents may have a role in these chronic diseases. To return to our original question: ‘Could Helicobacter Organisms Cause IBD?’ The question as written is a deceit for its simplicity, and taken literally the answer must be ‘no.’ Expanding upon the question, it is possible to hypothesize that Helicobacter spp. could play a role, perhaps a very important role, in variants of IBD. We believe that the most likely involvement would be as an orchestrator in the switch from a ‘healthy’ colonic microbiota to dysbiosis, rather than as a chronic infection.