Fatores de crescimento presentes no miocárdio de pacientes com cardiopatia chagásica crônica

Abstract

In this work we quantified various growth factors in the myocardium of 19 patients with chronic chagasic cardiomyopathy and heart failure, through the immunoperoxidase technique. We looked for T. cruzi antigens, growth factors (GM-CSF, TGF-beta1, PDGF-A and PDGF-B) and inflammatory cells (CD4+, CD8+, CD20+ and CD68+). The mean ratio of CD4+/CD8+ T lymphocytes was 0.6 +/- 0.3. The mean number of positive interstitial cells was 5.9 +/- 3.1 for CD68+ (macrophages); 7.5 +/- 4.3 for PDGF-A+; 2.9 +/- 2.7 for PDGF-B+, 2.2 +/- 1.9 for TGF-beta1+ and 2.3 +/- 1.9 for GM-CSF+. The immunoreaction for PDGF-A was intense, occurring also in the endothelium, smooth muscle cells and the sarcolemma; there was no correlation between the number of positive interstitial cells and the semiquantitation of the same growth factors in the other cells. TGF-beta1 presented low expression in 100% of the cases. In conclusion, PDGF-A and B are probably the growth factors most related to the proliferative lesions and fibrosis present in chronic chagasic cardiomyopathy. GM-CSF and TGF-beta1 are present in low levels. There was no statistical correlation between growth factors and the quantity of the parasitic antigens.

Moderate physical exercise reduces parasitaemia and protects colonic myenteric neurons in mice infected with Trypanosoma cruzi

“…Animals in the TI group exhibited an 18.0% increase in the synthesis of TGFb, with a 'large effect' of 0.7 (TI 9 SI), emphasizing the importance of moderate physical exercise in the regulation and control of the activation of immune system macrophages in response to physiological changes that result from T. cruzi infection. Necropsy fragments of the myocardium in humans with chronic Chagas' disease and congestive heart failure had little expression of TGF-b, suggesting that an inhibitory factor may have acted on macrophages, which may correspond to immunodepression caused by the presence of T. cruzi (Reis et al 2000).…”

Developments in the management of Chagas cardiomyopathy

“…[35] Moreover, TGF-β modulates the cardiac myocyte phenotype and triggers hypertrophic effects. [35,36] In the myocardium of Chagas disease patients, there are increased levels of TGF-β and other growth factors, such as granulocyte-macrophage-colony-stimulating factor and platelet-derived growth factor [37] that may mediate fibrosis. In a retrospective study of 54 Chagas disease patients, TGF-β1 was independently associated with all-cause mortality and hospitalization due to heart failure or cardiac arrhythmias.…”

Correlation of transforming growth factor-β1 and tumour necrosis factor levels with left ventricular function in Chagas disease

“…Histopathological studies found no increase in myocardial TGF-β1 mRNA expression in patients with Chagas heart disease compared to in non-infected subjects ( Nogueira et al 2014 ). Others also found a low prevalence of TGF-β1-positive cells within the myocardium of patients with Chagas disease and HF ( Reis et al 2000 ). The number of TGF-β-producing inflammatory cells within the myocardium was also found to be similar between patients with Chagas disease cardiac form with or without HF ( Rodrigues et al 2012 ).…”