Inflammatory diseases may have a role in the pathogenesis of atherosclerosis. Several epidemiological and clinical studies have explored the possible association between Helicobacter pylori seropositivity, cardiovascular risk factors, and ischemic heart disease. The contradictory results of these studies have fueled a debate regarding the link between H pylori infection and atherogenesis. This study tested the hypothesis that H pylori infection might influence atherosclerosis in vivo in mice. Male wild-type C57/Bl6 mice and LDL-receptor deficient congenic mice were randomly assigned for infection with H pylori. All animals were fed a high-cholesterol diet (1.25%) for 6 or 12 weeks. At autopsy, we compared aortic atherosclerotic lesion formation and lipid deposition. H pylori infection influenced neither the progression of atherosclerotic lesions nor lipid deposition. Moreover, the cellularity of atherosclerotic lesions (macrophages and T cells) did not differ between mice infected or not infected with H pylori. This in vivo study performed in a mouse model of atherosclerosis revealed no indication that H pylori infection might contribute to the development of atherosclerotic lesion formation. The full text of this article is available at http://www.circresaha.org.