Infectious agents and autoimmunity in acute coronary atherothrombosis

Our understanding of the pathogenesis of the acute thrombotic complications of the atherosclerosis has burgeoned in recent years. We now understand that many acute thrombotic coronary occlusions do not necessarily result from critically stenosed sites in the arteries. This distinction between lesions versus lumen diameter challenges our traditional reliance upon coronary anatomy. Atherothrombosis is the major determinant of acute ischemic cardiovascular events, such as myocardial infarction and stroke. Thus, its understanding is essential to enable the development of targeted and more effective therapies. Although related in part to alterations in lipid metabolism, atherosclerosis is now considered a primarily immune-mediated disease/Upon searching the literature, we found that it is has been recently proposed that chronic infections can contribute to the development of atheromas either directly (endothelial injury, invasion of endothelial cells and platelet aggregation) or indirectly (production of antibodies to lipopolysaccharide, cytokines and dysfunction of the immune system).In response to infection (e.g., oral bacteria among others), the immune system jumps into action, deploying cells as well as antibodies in order to recognize and destroy the invaders. Antibodies are molecules produced by plasma cells and B cells against the “enemy” – the infectious agent. However, owing to molecular mimicry or antigenic similarity between these infectious agents and human tissue structure, in a genetically susceptible individual, components of the body’s immune system target one or more types of the person’s own tissue, which may result in autoimmunity. Evidence indicates that infectious agents play a pivotal role in the induction of autoimmunities. The question of how infectious agents contribute to autoimmunity has continued to be of interest to clinical and basic researchers and immunologists in general/In many cases, it is not a single infection but rather the “burden of infections” from childhood that is responsible for the induction of autoimmunity. Taking together the above presented data, it appears that pathogens, through the release of toxins, seem to be capable of inducing changes in the host proteins. These can be recognized by the immune system, triggering an inflammatory process associated with the clinical manifestation of atherosclerosis – acute myocardial infarction. This and other immunopathogenic mechanisms need to be further elucidated.