Chronic Trypanosoma cruzi-elicited cardiomyopathy: from the discovery to the proposal of rational therapeutic interventions targeting cell adhesion molecules and chemokine receptors--how to make a dream come true.
One hundred years ago, Carlos Chagas discovered a new disease, the American trypanosomiasis. Chagas and co-workers later characterised the disease's common manifestation, chronic cardiomyopathy, and suggested that parasitic persistence coupled with inflammation was the key underlying pathogenic mechanism. Better comprehension of the molecular mechanisms leading to clinical heart afflictions is a prerequisite to developing new therapies that ameliorate inflammation and improve heart function without hampering parasite control. Here, we review recent data showing that distinct cell adhesion molecules, chemokines and chemokine receptors participate in anti-parasite immunity and/or detrimental leukocyte trafficking to the heart. Moreover, we offer evidence that CC-chemokine receptors may be attractive therapeutic targets aiming to regain homeostatic balance in parasite/host interaction thereby improving prognosis, supporting that it is becoming a non-phantasious proposal.
Lannes-Vieira
Joseli
J
Programa Integrado de Doença de Chagas, Fiocruz, Rio de Janeiro, RJ, Brasil. lannes@ioc.fiocruz.br
Silverio
Jaline Coutinho
JC
Pereira
Isabela Resende
IR
Vinagre
Nathália Ferreira
NF
Carvalho
Cristiano Marcelo Espinola
CM
Paiva
Cláudia Neto
CN
Silva da
Andréa Alice
AA
D000818:Animals; D016516:CD4-CD8 Ratio; D015815:Cell Adhesion Molecules / Q000276:immunology*; D002465:Cell Movement; D002598:Chagas Cardiomyopathy / Q000276:immunology* / Q000628:therapy; D002908:Chronic Disease; D009205:Myocarditis / Q000276:immunology* / Q000469:parasitology; D019707:Receptors, Chemokine / Q000276:immunology*; D014349:Trypanosoma cruzi / Q000276:immunology* / Q000472:pathogenicity
D015815:Cell Adhesion Molecules; D019707:Receptors, Chemokine