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Ricardo T. Gazzinelli - One of the best experts on this subject based on the ideXlab platform.
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Inducible Nitric Oxide Synthase in Heart Tissue and Nitric Oxide in Serum of Trypanosoma cruzi-Infected Rhesus Monkeys: Association with Heart Injury
PLoS neglected tropical diseases, 2012Co-Authors: Cristiano Marcelo Espinola Carvalho, Jaline Coutinho Silverio, Isabela Resende Pereira, Andrea Alice Da Silva, Otacı́lio Cruz Moreira, Renato Sergio Marchevsky, Janice Mery Chicarino De Oliveira Coelho, Constança Britto, Sérgio Salles Xavier, Ricardo T. GazzinelliAbstract:Background: The factors contributing to chronic Chagas' Heart disease remain unknown. High nitric oxide (NO) levels have been shown to be associated with cardiomyopathy severity in patients. Further, NO produced via inducible nitric oxide synthase (iNOS/NOS2) is proposed to play a role in Trypanosoma cruzi control. However, the participation of iNOS/NOS2 and NO in T. cruzi control and Heart Injury has been questioned. Here, using chronically infected rhesus monkeys and iNOS/NOS2-deficient (Nos2−/−) mice we explored the participation of iNOS/NOS2-derived NO in Heart Injury in T. cruzi infection. Methodology: Rhesus monkeys and C57BL/6 and Nos2−/− mice were infected with the Colombian T. cruzi strain. Parasite DNA was detected by polymerase chain reaction, T. cruzi antigens and iNOS/NOS2+ cells were immunohistochemically detected in Heart sections and NO levels in serum were determined by Griess reagent. Heart Injury was assessed by electrocardiogram (ECG), echocardiogram (ECHO), creatine kinase Heart isoenzyme (CK-MB) activity levels in serum and connexin 43 (Cx43) expression in the cardiac tissue. Results: Chronically infected monkeys presented conduction abnormalities, cardiac inflammation and fibrosis, which resembled the spectrum of human chronic chagasic cardiomyopathy (CCC). Importantly, chronic myocarditis was associated with parasite persistence. Moreover, Cx43 loss and increased CK-MB activity levels were primarily correlated with iNOS/NOS2+ cells infiltrating the cardiac tissue and NO levels in serum. Studies in Nos2−/− mice reinforced that the iNOS/NOS2-NO pathway plays a pivotal role in T. cruzi-elicited cardiomyocyte Injury and in conduction abnormalities that were associated with Cx43 loss in the cardiac tissue. Conclusion: T. cruzi-infected rhesus monkeys reproduce features of CCC. Moreover, our data support that in T. cruzi infection persistent parasite-triggered iNOS/NOS2 in the cardiac tissue and NO overproduction might contribute to CCC severity, mainly disturbing of the molecular pathway involved in electrical synchrony. These findings open a new avenue for therapeutic tools in Chagas' Heart disease.
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CD8+ T-cells expressing interferon gamma or perforin play antagonistic roles in Heart Injury in experimental Trypanosoma cruzi-elicited cardiomyopathy.
PLoS pathogens, 2012Co-Authors: Jaline Coutinho Silverio, Isabela Resende Pereira, Márcio Da Costa Cipitelli, Nathália Ferreira Vinagre, Mauricio M. Rodrigues, Ricardo T. Gazzinelli, Joseli Lannes-vieiraAbstract:In Chagas disease, CD8+ T-cells are critical for the control of Trypanosoma cruzi during acute infection. Conversely, CD8+ T-cell accumulation in the myocardium during chronic infection may cause tissue Injury leading to chronic chagasic cardiomyopathy (CCC). Here we explored the role of CD8+ T-cells in T. cruzi-elicited Heart Injury in C57BL/6 mice infected with the Colombian strain. Cardiomyocyte lesion evaluated by creatine kinase-MB isoenzyme activity levels in the serum and electrical abnormalities revealed by electrocardiogram were not associated with the intensity of Heart parasitism and myocarditis in the chronic infection. Further, there was no association between Heart Injury and systemic anti-T. cruzi CD8+ T-cell capacity to produce interferon-gamma (IFNγ) and to perform specific cytotoxicity. Heart Injury, however, paralleled accumulation of anti-T. cruzi cells in the cardiac tissue. In T. cruzi infection, most of the CD8+ T-cells segregated into IFNγ+ perforin (Pfn)neg or IFNγnegPfn+ cell populations. Colonization of the cardiac tissue by anti-T. cruzi CD8+Pfn+ cells paralleled the worsening of CCC. The adoptive cell transfer to T. cruzi-infected cd8−/− recipients showed that the CD8+ cells from infected ifnγ−/−pfn+/+ donors migrate towards the cardiac tissue to a greater extent and caused a more severe cardiomyocyte lesion than CD8+ cells from ifnγ+/+pfn−/− donors. Moreover, the reconstitution of naive cd8−/− mice with CD8+ cells from naive ifnγ+/+pfn−/− donors ameliorated T. cruzi-elicited Heart Injury paralleled IFNγ+ cells accumulation, whereas reconstitution with CD8+ cells from naive ifnγ−/−pfn+/+ donors led to an aggravation of the cardiomyocyte lesion, which was associated with the accumulation of Pfn+ cells in the cardiac tissue. Our data support a possible antagonist effect of CD8+Pfn+ and CD8+IFNγ+ cells during CCC. CD8+IFNγ+ cells may exert a beneficial role, whereas CD8+Pfn+ may play a detrimental role in T. cruzi-elicited Heart Injury.
Jaline Coutinho Silverio - One of the best experts on this subject based on the ideXlab platform.
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Inducible Nitric Oxide Synthase in Heart Tissue and Nitric Oxide in Serum of Trypanosoma cruzi-Infected Rhesus Monkeys: Association with Heart Injury
2016Co-Authors: Cristiano Marcelo, Jaline Coutinho Silverio, Espinola Carvalho, Andrea Alice Da Silva, Resende Pereira, Janice Mery, Chicarino Coelho, Constança Carvalho Britto, Otacı́lio Cruz Moreira, Renato Sergio MarchevskyAbstract:Background: The factors contributing to chronic Chagas ’ Heart disease remain unknown. High nitric oxide (NO) levels have been shown to be associated with cardiomyopathy severity in patients. Further, NO produced via inducible nitric oxide synthase (iNOS/NOS2) is proposed to play a role in Trypanosoma cruzi control. However, the participation of iNOS/NOS2 and NO in T. cruzi control and Heart Injury has been questioned. Here, using chronically infected rhesus monkeys and iNOS/ NOS2-deficient (Nos22/2) mice we explored the participation of iNOS/NOS2-derived NO in Heart Injury in T. cruzi infection. Methodology: Rhesus monkeys and C57BL/6 and Nos22/2 mice were infected with the Colombian T. cruzi strain. Parasite DNA was detected by polymerase chain reaction, T. cruzi antigens and iNOS/NOS2+ cells were immunohistochemically detected in Heart sections and NO levels in serum were determined by Griess reagent. Heart Injury was assessed by electrocardiogram (ECG), echocardiogram (ECHO), creatine kinase Heart isoenzyme (CK-MB) activity levels in serum an
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Inducible Nitric Oxide Synthase in Heart Tissue and Nitric Oxide in Serum of Trypanosoma cruzi-Infected Rhesus Monkeys: Association with Heart Injury
PLoS neglected tropical diseases, 2012Co-Authors: Cristiano Marcelo Espinola Carvalho, Jaline Coutinho Silverio, Isabela Resende Pereira, Andrea Alice Da Silva, Otacı́lio Cruz Moreira, Renato Sergio Marchevsky, Janice Mery Chicarino De Oliveira Coelho, Constança Britto, Sérgio Salles Xavier, Ricardo T. GazzinelliAbstract:Background: The factors contributing to chronic Chagas' Heart disease remain unknown. High nitric oxide (NO) levels have been shown to be associated with cardiomyopathy severity in patients. Further, NO produced via inducible nitric oxide synthase (iNOS/NOS2) is proposed to play a role in Trypanosoma cruzi control. However, the participation of iNOS/NOS2 and NO in T. cruzi control and Heart Injury has been questioned. Here, using chronically infected rhesus monkeys and iNOS/NOS2-deficient (Nos2−/−) mice we explored the participation of iNOS/NOS2-derived NO in Heart Injury in T. cruzi infection. Methodology: Rhesus monkeys and C57BL/6 and Nos2−/− mice were infected with the Colombian T. cruzi strain. Parasite DNA was detected by polymerase chain reaction, T. cruzi antigens and iNOS/NOS2+ cells were immunohistochemically detected in Heart sections and NO levels in serum were determined by Griess reagent. Heart Injury was assessed by electrocardiogram (ECG), echocardiogram (ECHO), creatine kinase Heart isoenzyme (CK-MB) activity levels in serum and connexin 43 (Cx43) expression in the cardiac tissue. Results: Chronically infected monkeys presented conduction abnormalities, cardiac inflammation and fibrosis, which resembled the spectrum of human chronic chagasic cardiomyopathy (CCC). Importantly, chronic myocarditis was associated with parasite persistence. Moreover, Cx43 loss and increased CK-MB activity levels were primarily correlated with iNOS/NOS2+ cells infiltrating the cardiac tissue and NO levels in serum. Studies in Nos2−/− mice reinforced that the iNOS/NOS2-NO pathway plays a pivotal role in T. cruzi-elicited cardiomyocyte Injury and in conduction abnormalities that were associated with Cx43 loss in the cardiac tissue. Conclusion: T. cruzi-infected rhesus monkeys reproduce features of CCC. Moreover, our data support that in T. cruzi infection persistent parasite-triggered iNOS/NOS2 in the cardiac tissue and NO overproduction might contribute to CCC severity, mainly disturbing of the molecular pathway involved in electrical synchrony. These findings open a new avenue for therapeutic tools in Chagas' Heart disease.
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CD8+ T-cells expressing interferon gamma or perforin play antagonistic roles in Heart Injury in experimental Trypanosoma cruzi-elicited cardiomyopathy.
PLoS pathogens, 2012Co-Authors: Jaline Coutinho Silverio, Isabela Resende Pereira, Márcio Da Costa Cipitelli, Nathália Ferreira Vinagre, Mauricio M. Rodrigues, Ricardo T. Gazzinelli, Joseli Lannes-vieiraAbstract:In Chagas disease, CD8+ T-cells are critical for the control of Trypanosoma cruzi during acute infection. Conversely, CD8+ T-cell accumulation in the myocardium during chronic infection may cause tissue Injury leading to chronic chagasic cardiomyopathy (CCC). Here we explored the role of CD8+ T-cells in T. cruzi-elicited Heart Injury in C57BL/6 mice infected with the Colombian strain. Cardiomyocyte lesion evaluated by creatine kinase-MB isoenzyme activity levels in the serum and electrical abnormalities revealed by electrocardiogram were not associated with the intensity of Heart parasitism and myocarditis in the chronic infection. Further, there was no association between Heart Injury and systemic anti-T. cruzi CD8+ T-cell capacity to produce interferon-gamma (IFNγ) and to perform specific cytotoxicity. Heart Injury, however, paralleled accumulation of anti-T. cruzi cells in the cardiac tissue. In T. cruzi infection, most of the CD8+ T-cells segregated into IFNγ+ perforin (Pfn)neg or IFNγnegPfn+ cell populations. Colonization of the cardiac tissue by anti-T. cruzi CD8+Pfn+ cells paralleled the worsening of CCC. The adoptive cell transfer to T. cruzi-infected cd8−/− recipients showed that the CD8+ cells from infected ifnγ−/−pfn+/+ donors migrate towards the cardiac tissue to a greater extent and caused a more severe cardiomyocyte lesion than CD8+ cells from ifnγ+/+pfn−/− donors. Moreover, the reconstitution of naive cd8−/− mice with CD8+ cells from naive ifnγ+/+pfn−/− donors ameliorated T. cruzi-elicited Heart Injury paralleled IFNγ+ cells accumulation, whereas reconstitution with CD8+ cells from naive ifnγ−/−pfn+/+ donors led to an aggravation of the cardiomyocyte lesion, which was associated with the accumulation of Pfn+ cells in the cardiac tissue. Our data support a possible antagonist effect of CD8+Pfn+ and CD8+IFNγ+ cells during CCC. CD8+IFNγ+ cells may exert a beneficial role, whereas CD8+Pfn+ may play a detrimental role in T. cruzi-elicited Heart Injury.
Isabela Resende Pereira - One of the best experts on this subject based on the ideXlab platform.
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Inducible Nitric Oxide Synthase in Heart Tissue and Nitric Oxide in Serum of Trypanosoma cruzi-Infected Rhesus Monkeys: Association with Heart Injury
PLoS neglected tropical diseases, 2012Co-Authors: Cristiano Marcelo Espinola Carvalho, Jaline Coutinho Silverio, Isabela Resende Pereira, Andrea Alice Da Silva, Otacı́lio Cruz Moreira, Renato Sergio Marchevsky, Janice Mery Chicarino De Oliveira Coelho, Constança Britto, Sérgio Salles Xavier, Ricardo T. GazzinelliAbstract:Background: The factors contributing to chronic Chagas' Heart disease remain unknown. High nitric oxide (NO) levels have been shown to be associated with cardiomyopathy severity in patients. Further, NO produced via inducible nitric oxide synthase (iNOS/NOS2) is proposed to play a role in Trypanosoma cruzi control. However, the participation of iNOS/NOS2 and NO in T. cruzi control and Heart Injury has been questioned. Here, using chronically infected rhesus monkeys and iNOS/NOS2-deficient (Nos2−/−) mice we explored the participation of iNOS/NOS2-derived NO in Heart Injury in T. cruzi infection. Methodology: Rhesus monkeys and C57BL/6 and Nos2−/− mice were infected with the Colombian T. cruzi strain. Parasite DNA was detected by polymerase chain reaction, T. cruzi antigens and iNOS/NOS2+ cells were immunohistochemically detected in Heart sections and NO levels in serum were determined by Griess reagent. Heart Injury was assessed by electrocardiogram (ECG), echocardiogram (ECHO), creatine kinase Heart isoenzyme (CK-MB) activity levels in serum and connexin 43 (Cx43) expression in the cardiac tissue. Results: Chronically infected monkeys presented conduction abnormalities, cardiac inflammation and fibrosis, which resembled the spectrum of human chronic chagasic cardiomyopathy (CCC). Importantly, chronic myocarditis was associated with parasite persistence. Moreover, Cx43 loss and increased CK-MB activity levels were primarily correlated with iNOS/NOS2+ cells infiltrating the cardiac tissue and NO levels in serum. Studies in Nos2−/− mice reinforced that the iNOS/NOS2-NO pathway plays a pivotal role in T. cruzi-elicited cardiomyocyte Injury and in conduction abnormalities that were associated with Cx43 loss in the cardiac tissue. Conclusion: T. cruzi-infected rhesus monkeys reproduce features of CCC. Moreover, our data support that in T. cruzi infection persistent parasite-triggered iNOS/NOS2 in the cardiac tissue and NO overproduction might contribute to CCC severity, mainly disturbing of the molecular pathway involved in electrical synchrony. These findings open a new avenue for therapeutic tools in Chagas' Heart disease.
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CD8+ T-cells expressing interferon gamma or perforin play antagonistic roles in Heart Injury in experimental Trypanosoma cruzi-elicited cardiomyopathy.
PLoS pathogens, 2012Co-Authors: Jaline Coutinho Silverio, Isabela Resende Pereira, Márcio Da Costa Cipitelli, Nathália Ferreira Vinagre, Mauricio M. Rodrigues, Ricardo T. Gazzinelli, Joseli Lannes-vieiraAbstract:In Chagas disease, CD8+ T-cells are critical for the control of Trypanosoma cruzi during acute infection. Conversely, CD8+ T-cell accumulation in the myocardium during chronic infection may cause tissue Injury leading to chronic chagasic cardiomyopathy (CCC). Here we explored the role of CD8+ T-cells in T. cruzi-elicited Heart Injury in C57BL/6 mice infected with the Colombian strain. Cardiomyocyte lesion evaluated by creatine kinase-MB isoenzyme activity levels in the serum and electrical abnormalities revealed by electrocardiogram were not associated with the intensity of Heart parasitism and myocarditis in the chronic infection. Further, there was no association between Heart Injury and systemic anti-T. cruzi CD8+ T-cell capacity to produce interferon-gamma (IFNγ) and to perform specific cytotoxicity. Heart Injury, however, paralleled accumulation of anti-T. cruzi cells in the cardiac tissue. In T. cruzi infection, most of the CD8+ T-cells segregated into IFNγ+ perforin (Pfn)neg or IFNγnegPfn+ cell populations. Colonization of the cardiac tissue by anti-T. cruzi CD8+Pfn+ cells paralleled the worsening of CCC. The adoptive cell transfer to T. cruzi-infected cd8−/− recipients showed that the CD8+ cells from infected ifnγ−/−pfn+/+ donors migrate towards the cardiac tissue to a greater extent and caused a more severe cardiomyocyte lesion than CD8+ cells from ifnγ+/+pfn−/− donors. Moreover, the reconstitution of naive cd8−/− mice with CD8+ cells from naive ifnγ+/+pfn−/− donors ameliorated T. cruzi-elicited Heart Injury paralleled IFNγ+ cells accumulation, whereas reconstitution with CD8+ cells from naive ifnγ−/−pfn+/+ donors led to an aggravation of the cardiomyocyte lesion, which was associated with the accumulation of Pfn+ cells in the cardiac tissue. Our data support a possible antagonist effect of CD8+Pfn+ and CD8+IFNγ+ cells during CCC. CD8+IFNγ+ cells may exert a beneficial role, whereas CD8+Pfn+ may play a detrimental role in T. cruzi-elicited Heart Injury.
Renato Sergio Marchevsky - One of the best experts on this subject based on the ideXlab platform.
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Inducible Nitric Oxide Synthase in Heart Tissue and Nitric Oxide in Serum of Trypanosoma cruzi-Infected Rhesus Monkeys: Association with Heart Injury
2016Co-Authors: Cristiano Marcelo, Jaline Coutinho Silverio, Espinola Carvalho, Andrea Alice Da Silva, Resende Pereira, Janice Mery, Chicarino Coelho, Constança Carvalho Britto, Otacı́lio Cruz Moreira, Renato Sergio MarchevskyAbstract:Background: The factors contributing to chronic Chagas ’ Heart disease remain unknown. High nitric oxide (NO) levels have been shown to be associated with cardiomyopathy severity in patients. Further, NO produced via inducible nitric oxide synthase (iNOS/NOS2) is proposed to play a role in Trypanosoma cruzi control. However, the participation of iNOS/NOS2 and NO in T. cruzi control and Heart Injury has been questioned. Here, using chronically infected rhesus monkeys and iNOS/ NOS2-deficient (Nos22/2) mice we explored the participation of iNOS/NOS2-derived NO in Heart Injury in T. cruzi infection. Methodology: Rhesus monkeys and C57BL/6 and Nos22/2 mice were infected with the Colombian T. cruzi strain. Parasite DNA was detected by polymerase chain reaction, T. cruzi antigens and iNOS/NOS2+ cells were immunohistochemically detected in Heart sections and NO levels in serum were determined by Griess reagent. Heart Injury was assessed by electrocardiogram (ECG), echocardiogram (ECHO), creatine kinase Heart isoenzyme (CK-MB) activity levels in serum an
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Inducible Nitric Oxide Synthase in Heart Tissue and Nitric Oxide in Serum of Trypanosoma cruzi-Infected Rhesus Monkeys: Association with Heart Injury
PLoS neglected tropical diseases, 2012Co-Authors: Cristiano Marcelo Espinola Carvalho, Jaline Coutinho Silverio, Isabela Resende Pereira, Andrea Alice Da Silva, Otacı́lio Cruz Moreira, Renato Sergio Marchevsky, Janice Mery Chicarino De Oliveira Coelho, Constança Britto, Sérgio Salles Xavier, Ricardo T. GazzinelliAbstract:Background: The factors contributing to chronic Chagas' Heart disease remain unknown. High nitric oxide (NO) levels have been shown to be associated with cardiomyopathy severity in patients. Further, NO produced via inducible nitric oxide synthase (iNOS/NOS2) is proposed to play a role in Trypanosoma cruzi control. However, the participation of iNOS/NOS2 and NO in T. cruzi control and Heart Injury has been questioned. Here, using chronically infected rhesus monkeys and iNOS/NOS2-deficient (Nos2−/−) mice we explored the participation of iNOS/NOS2-derived NO in Heart Injury in T. cruzi infection. Methodology: Rhesus monkeys and C57BL/6 and Nos2−/− mice were infected with the Colombian T. cruzi strain. Parasite DNA was detected by polymerase chain reaction, T. cruzi antigens and iNOS/NOS2+ cells were immunohistochemically detected in Heart sections and NO levels in serum were determined by Griess reagent. Heart Injury was assessed by electrocardiogram (ECG), echocardiogram (ECHO), creatine kinase Heart isoenzyme (CK-MB) activity levels in serum and connexin 43 (Cx43) expression in the cardiac tissue. Results: Chronically infected monkeys presented conduction abnormalities, cardiac inflammation and fibrosis, which resembled the spectrum of human chronic chagasic cardiomyopathy (CCC). Importantly, chronic myocarditis was associated with parasite persistence. Moreover, Cx43 loss and increased CK-MB activity levels were primarily correlated with iNOS/NOS2+ cells infiltrating the cardiac tissue and NO levels in serum. Studies in Nos2−/− mice reinforced that the iNOS/NOS2-NO pathway plays a pivotal role in T. cruzi-elicited cardiomyocyte Injury and in conduction abnormalities that were associated with Cx43 loss in the cardiac tissue. Conclusion: T. cruzi-infected rhesus monkeys reproduce features of CCC. Moreover, our data support that in T. cruzi infection persistent parasite-triggered iNOS/NOS2 in the cardiac tissue and NO overproduction might contribute to CCC severity, mainly disturbing of the molecular pathway involved in electrical synchrony. These findings open a new avenue for therapeutic tools in Chagas' Heart disease.
Cristiano Marcelo Espinola Carvalho - One of the best experts on this subject based on the ideXlab platform.
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Inducible Nitric Oxide Synthase in Heart Tissue and Nitric Oxide in Serum of Trypanosoma cruzi-Infected Rhesus Monkeys: Association with Heart Injury
PLoS neglected tropical diseases, 2012Co-Authors: Cristiano Marcelo Espinola Carvalho, Jaline Coutinho Silverio, Isabela Resende Pereira, Andrea Alice Da Silva, Otacı́lio Cruz Moreira, Renato Sergio Marchevsky, Janice Mery Chicarino De Oliveira Coelho, Constança Britto, Sérgio Salles Xavier, Ricardo T. GazzinelliAbstract:Background: The factors contributing to chronic Chagas' Heart disease remain unknown. High nitric oxide (NO) levels have been shown to be associated with cardiomyopathy severity in patients. Further, NO produced via inducible nitric oxide synthase (iNOS/NOS2) is proposed to play a role in Trypanosoma cruzi control. However, the participation of iNOS/NOS2 and NO in T. cruzi control and Heart Injury has been questioned. Here, using chronically infected rhesus monkeys and iNOS/NOS2-deficient (Nos2−/−) mice we explored the participation of iNOS/NOS2-derived NO in Heart Injury in T. cruzi infection. Methodology: Rhesus monkeys and C57BL/6 and Nos2−/− mice were infected with the Colombian T. cruzi strain. Parasite DNA was detected by polymerase chain reaction, T. cruzi antigens and iNOS/NOS2+ cells were immunohistochemically detected in Heart sections and NO levels in serum were determined by Griess reagent. Heart Injury was assessed by electrocardiogram (ECG), echocardiogram (ECHO), creatine kinase Heart isoenzyme (CK-MB) activity levels in serum and connexin 43 (Cx43) expression in the cardiac tissue. Results: Chronically infected monkeys presented conduction abnormalities, cardiac inflammation and fibrosis, which resembled the spectrum of human chronic chagasic cardiomyopathy (CCC). Importantly, chronic myocarditis was associated with parasite persistence. Moreover, Cx43 loss and increased CK-MB activity levels were primarily correlated with iNOS/NOS2+ cells infiltrating the cardiac tissue and NO levels in serum. Studies in Nos2−/− mice reinforced that the iNOS/NOS2-NO pathway plays a pivotal role in T. cruzi-elicited cardiomyocyte Injury and in conduction abnormalities that were associated with Cx43 loss in the cardiac tissue. Conclusion: T. cruzi-infected rhesus monkeys reproduce features of CCC. Moreover, our data support that in T. cruzi infection persistent parasite-triggered iNOS/NOS2 in the cardiac tissue and NO overproduction might contribute to CCC severity, mainly disturbing of the molecular pathway involved in electrical synchrony. These findings open a new avenue for therapeutic tools in Chagas' Heart disease.
