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1 Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA, USA; Division of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA
2 Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA, USA
3 Department of Medicine and Division of Gastroenterology, Brigham and Women's Hospital and Harvard Digestive Diseases Center, Harvard Medical School, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: kmaurer{at}mit.edu.
Recently we demonstrated that cholesterol gallstone prone C57L/J mice rarely develop gallstones unless they are infected with certain cholelithogenic enterohepatic Helicobacter species. Since the common gastric pathogen H. pylori has been identified in the hepatobiliary tree of cholesterol gallstone patients, we wished to ascertain if H. pylori is cholelithogenic, by prospectively studying C57L infected mice fed a lithogenic diet. Weanling, Helicobacter spp.-free male C57L mice were either infected with H. pylori SS1 or sham dosed. Mice were then fed a lithogenic diet (1.0% cholesterol, 0.5% cholic acid and 15% dairy triglycerides) for eight weeks. At 16-weeks of age, mice were euthanatized, the biliary phenotype was analyzed microscopically, and tissues were analyzed histopathologically. H. pylori infection did not promote cholesterol monohydrate crystal formation (20% vs. 10%), sandy stone formation (0% for both) nor true gallstone formation (20%) when compared to uninfected mice fed the lithogenic diet (10%). Additionally, H. pylori failed to stimulate mucin gel accumulation in the gallbladder or alter gallbladder size when compared with uninfected animals. H. pylori infected C57L mice developed moderate to severe gastritis by 12 weeks and the lithogenic diet itself produced lesions in the forestomach which were exacerbated by the infection. We conclude that H. pylori infection does not play any role in murine cholesterol gallstone formation. Nonetheless, the C57L mouse develops severe lesions of both the glandular and non-glandular stomach in response to H. pylori infection and the lithogenic diet respectively.
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