Anti-Glycan Autoantibodies Induced by as a Potential Risk Factor for Myocardial Infarction.

A number of epidemiological studies have evaluated the potential association between and cardiovascular disease, but with contrasting results. We have previously shown that infection is able to induce in mice and humans autoantibodies cross-reacting with histo-blood group Lewis antigens, expressed in different organs and in plasma glycoproteins and glycolipids. The aim of this study was to assess whether immunization of animals with might induce myocardial histopathological changes. We have retrospectively examined, in detail, the histology of archived organs from mice and rabbits immunized with in our previous studies. Human sera and cross-reacting monoclonal antibodies were also tested against bacterial preparations and tissue sections. Areas of myocardial necrosis, associated with coronary thrombotic occlusion, were found in 5 of 20 mice and 2 of 5 rabbits previously immunized with suspensions of . No similar lesions were found in control animals, suggesting a causal link with immunization. The animals bearing myocardial lesions had not been infected but only immunized months earlier with parenteral injections of dead cells. This strongly suggests that immunization, by itself, might play a causative role. We propose that the cross-reactive autoimmune response induced by could promote thrombotic occlusion through direct endothelial damage or by perturbing the coagulation process.