The role of Helicobacter pylori in atherosclerosis may be related to the humoral response against specific protein antigens as well as to Lewis (Le) determinants present in the lipopolysaccharide (LPS) structure of such bacteria. The role of bacterial LPS in atherogenesis may also be related to the concentration of soluble CD14 (sCD14) and  LPS binding protein (LBP) in the circulation. We performed serologic studies in which the immunoglobuline: IgG and IgA to glycine acid extract-GE of H. pylori surface antigens, IgG to  H. pylori LPSs with or without LeX or LeXY determinants, immune complexes (ICs) LeX-anti-LeX IgG and LeY-anti-LeY IgG, and nonimmunoglobuline markers: sCD14 and LBP of host response to LPS were estimated. The investigated group consisted of 140 patients with coronary artery disease (CAD), hospitalized due to myocardial infarction (34) or unstable angina pectoris (106). The control group consisted of 60 symptomless volunteers. The H. pylori infection was detected with high prevalence in CAD patients. The humoral response against H. pylori in CAD patients was characterized by higher prevalence of anti-GE IgG and IgA and by higher levels of anti-GE IgA, IgG to H. pylori LPS of LeXY(+) type and ICs LeY-anti-LeY IgG. The elevated LBP and sCD14 levels were found in CAD patients which was combined with H. pylori infection. The H. pylori LPS could be considered as a cofactor involved in atherogenesis by inducing strong humoral response to LeXY determinants and by increased levels of sCD14 and LBP nonimmunoglobuline markers of host response to LPS.