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Helicobacter species can colonise the mammalian gastrointestinal and hepatobiliary tract which usually results in a chronic infection coupled to an inflammatory host response. It is therefore not surprising that colonisation with Helicobacter species is linked with a range of inflammation associated gastrointestinal and hepatobiliary diseases.1 Recently, this range has been expanded, with an association of infection with enterohepatic Helicobacter species and the formation of cholesterol gallstones.2 In their study, Maurer and colleagues2 demonstrated that murine infection with the enterohepatic Helicobacter species H bilis and H hepaticus accelerated the formation of cholesterol gallstones in mice fed a lithogenic diet. Although the gallbladder mucosa in mice with gallstones displayed signs of inflammation, Helicobacter species were not cultured from the inflamed gallbladder or bile. Therefore, Maurer et al hypothesised that the chronic immune stimulation caused by Helicobacter species, rather than a direct bacterial factor, led to the production of nucleating agents, thus indirectly linking

Urease induced calcium precipitation by Helicobacter species may initiate gallstone formation