title: Autonomic neuroimmunomodulation in chagasic cardiomyopathy.
abstract: Chagas disease is an endemic parasitic disease, caused by the flagellate protozoan Trypanosoma cruzi, with a high prevalence in Latin America. During its chronic phase, chronic chagasic cardiomyopathy 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 autoimmune diseases. However, nothing is known about this autonomic neural modulation of the immune response in Chagas disease. In the present report, we discuss several sets of evidence suggesting that changes in the autonomic drive directed towards 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.
authors.affiliation: Department of Biological Sciences, Triangulo Mineiro Federal University, Uberaba, MG, Brazil.
authors.forename: Marcus Paulo
authors.initials: MP
authors.lastname: Ribeiro Machado
authors.forename: Valdo Jose
authors.initials: VJ
authors.lastname: Dias da Silva
mesh_terms: D000818:Animals; D001341:Autonomic Nervous System / Q000276:immunology* / Q000503:physiopathology*; D002598:Chagas Cardiomyopathy / Q000276:immunology* / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology; D015213:Neuroimmunomodulation / Q000276:immunology* / Q000502:physiology*