Inflammatory diseases may have a role in the pathogenesis of atherosclerosis. Several epidemiological and clinical studies have explored the possible association betweenHelicobacter pyloriseropositivity, cardiovascular risk factors, and ischemic heart disease. The contradictory results of these studies have fueled a debate regarding the link betweenH pyloriinfection and atherogenesis. This study tested the hypothesis thatH pyloriinfection might influence atherosclerosis in vivo in mice. Male wild-type C57/Bl6 mice and LDL-receptor deficient congenic mice were randomly assigned for infection withH 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 pyloriinfection 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 withH pylori. This in vivo study performed in a mouse model of atherosclerosis revealed no indication thatH pyloriinfection might contribute to the development of atherosclerotic lesion formation. The full text of this article is available at http://www.circresaha.org.