Autonomic neuroimmunomodulation in chagasic cardiomyopathy.
ABSTRACT Chagas disease is an endemic parasitic disease caused by the flagellate protozoa Trypanosoma cruzi with a high prevalence in Latin America. During its chronic phase, chronic chagasic cardiomyopathy (CCC) is the most apparent clinical form, affecting 25-30% of patients. This clinical form may present as congestive heart failure, thromboembolic phenomena, cardiac arrhythmias and sudden death. Pathological findings in the heart include mononuclear inflammatory infiltrate, focal myocarditis, epicarditis and neuroganglionitis, associated with variable focal fibrosis and widely variable autonomic dysfunction. The immune-inflammatory response has been considered to be the cause of the autonomic dysfunction, which may trigger life-threatening arrhythmias and sudden death. In the last few years, several reports in the literature have described the marked role played by the autonomic nervous system in the modulation of the immune-inflammatory response in some experimental models of infectious, ischaemic and auto-immune diseases. However, nothing is known about this autonomic neural modulation on the immune response in Chagas disease. In this present report, we discuss several sets of evidence that suggest that changes in the autonomic drive directed toward the heart could modify blood and tissue parasitism as well as inflammatory infiltration in chagasic cardiomyopathy. The pathogenic implications of these potential neural immune manipulations are also discussed.