Interfer?ncia da dieta hipoprot?ica na s?ntese de Fractalquina/CX3CL1 e endotelina em modelo experimental de infec??o pelo Trypanosoma cruzi.

A cardiopatia chag?sica, desenvolvida ap?s a infec??o pelo Trypanosoma cruzi (T. cruzi) ? uma doen?a inflamat?ria cr?nica. Apresenta altera??es vasculares significativas, a ponto de conduzir o hospedeiro vertebrado ao ?bito. M?ltiplos fatores parecem contribuir para os eventos cardiovasculares na doen?a de Chagas, mas a resposta imune do hospedeiro aparece como essencial tanto em modelo humano quanto experimental. Em particular, a produ??o de quimiocinas e de outros mediadores inflamat?rios t?m apresentado grande relev?ncia na altera??o da homeostase e contribu?do para o recrutamento leucocit?rio, eventos primordiais para a patog?nese da doen?a de Chagas. Conhecendo-se a prec?ria situa??o nutricional das popula??es negligenciadas em ?reas end?micas para a doen?a de Chagas, e tamb?m a rela??o direta entre fatores nutricionais e a resposta imune do hospedeiro, este trabalho objetivou avaliar a interfer?ncia da defici?ncia prot?ica na resposta inflamat?ria card?aca em modelo experimental da doen?a de Chagas. Utilizando-se ratos Fisher machos, induzimos uma desnutri??o prot?ica nesses animais, seguida de infec??o pelo Trypanosoma cruzi (cepa Y) e avaliamos a s?ntese da quimiocina Fractalquina/CX3CL1 e do pept?deo endotelina associados ? les?o card?aca durante as fases aguda e cr?nica da doen?a de Chagas. Observou-se que a defici?ncia prot?ica foi capaz de potencializar a s?ntese sist?mica de CX3CL1 e de endotelina, tanto na fase aguda quanto cr?nica da doen?a de Chagas, por?m n?o foi capaz de controlar o aumento da carga parasit?ria na circula??o sangu?nea. Nossos dados mostram, pela primeira vez, a presen?a da CX3CL1 durante a infec??o pelo Trypanosoma cruzi. E ainda, demonstrou a import?ncia do estado nutricional do hospedeiro nas altera??es imunes, pertinentes ? doen?a de Chagas, no modelo experimental, sugerindo que a m?dio ou longo prazo, tais altera??es poderiam contribuir para a progress?o cl?nica da doen?a.Chagas' heart disease developed after Trypanosoma cruzi infection, is a chronic inflammatory disease. It presents significant vascular changes, the point of driving the vertebrate host to death. Multiple factors seem to contribute to cardiovascular events in Chaga's disease, but the host immune response appears to be essential both in human and experimental model. In particular, the production of chemokines and other inflammatory mediators have shown great importance in altering the homeostasis and contributing to leukocyte recruitment, events essential for the pathogenesis of the disease. Knowing the precarious nutritional situation of neglected populations in areas endemic for Chaga?s disease, and also the direct relationship between nutritional factors and host immune response, this study aimed to evaluate the role of protein deficiency in the inflammatory response rate during an experimental model of disease. Using Fisher male rats, we induced proteic malnutrition in these animals, followed by infection with Trypanosoma cruzi (Y strain) and evaluated the synthesis of the chemokine Fractalkine/CX3CL1 and peptide endothelin associated with cardiac injury during the acute and chronic phases of Chaga?s disease. It was observed that protein deficiency was able to enhance the systemic synthesis of CX3CL1 and endothelin in both acute and chronic Chaga?s disease, but was not able to control the increase in parasite load in the bloodstream. Our data show for the first time, the presence of CX3CL1 during infection with Trypanosoma cruzi. Also, we demonstrated the importance of nutritional status in the host immune changes, relevant to Chaga's disease in the experimental model, suggesting that the medium to long term, such changes could contribute to the progression of the disease