Differential apoptosis-like cell death in amastigote and trypomastigote forms from Trypanosoma cruzi-infected heart cells in vitro

Souza, Elen Mello de; Nefertiti, A. S. G.; Bailly, Christian; Lansiaux, Amélie; Soeiro, M. N. C.

doi:10.1007/s00441-010-0985-5

Cited by 19 publications

(23 citation statements)

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“…Apoptosis-like death has been reported in T. cruzi amastigote nests and trypomastigotes, and hypothesized to be the result of control of parasite burden regulated by the parasite itself or by the host, parasite evasion of the host immune response and clonal selection [13],[38]–[39]. However, these studies were conducted during the acute phase [13],[38], whereas we observed apoptosis-like death in nests during both the acute and chronic phases.…”

Section: Discussioncontrasting

confidence: 54%

Cell Death and Serum Markers of Collagen Metabolism during Cardiac Remodeling in Cavia porcellus Experimentally Infected with Trypanosoma cruzi

et al. 2013

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We studied cell death by apoptosis and necrosis in cardiac remodeling produced by Trypanosoma cruzi infection. In addition, we evaluated collagen I, III, IV (CI, CIII and CIV) deposition in cardiac tissue, and their relationship with serum levels of procollagen type I carboxy-terminal propeptide (PICP) and procollagen type III amino-terminal propeptide (PIIINP). Eight infected and two uninfected guinea pigs were necropsied at seven time points up to one year post-infection. Cell death by necrosis and apoptosis was determined by histopathological observation and terminal deoxynucleotidyl transferase dUTP nick end labeling, respectively. Deposition of cardiac collagen types was determined by immunohistochemistry and serum levels of PICP, PIIINP, and anti-T. cruzi IgG1 and IgG2 by ELISA. IgG2 (Th1 response) predominated throughout the course of infection; IgG1 (Th2 response) was detected during the chronic phase. Cardiac cell death by necrosis predominated over apoptosis during the acute phase; during the chronic phase, both apoptosis and necrosis were observed in cardiac cells. Apoptosis was also observed in lymphocytes, endothelial cells and epicardial adipose tissue, especially in the chronic phase. Cardiac levels of CI, CIII, CIV increased progressively, but the highest levels were seen in the chronic phase and were primarily due to increase in CIII and CIV. High serum levels of PICP and PIIINP were observed throughout the infection, and increased levels of both biomarkers were associated with cardiac fibrosis (p = 0.002 and p = 0.038, respectively). These results confirm the role of apoptosis in cell loss mainly during the chronic phase and the utility of PICP and PIIINP as biomarkers of fibrosis in cardiac remodeling during T. cruzi infection.

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Section: Discussioncontrasting

confidence: 54%

Cell Death and Serum Markers of Collagen Metabolism during Cardiac Remodeling in Cavia porcellus Experimentally Infected with Trypanosoma cruzi

et al. 2013

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“…Still, cardiomyocytes infected with T. cruzi clone Dm28c have higher levels of apoptosis compared to infection with strains Y and CL (de Souza et al, 2003). Furthermore, the intracellular parasites themselves also undergo apoptosis, hinting at a host attempt to control parasite burden (de Souza et al, 2003, 2010). Interestingly, it has been shown that α2-macroglobulin, a plasma proteinase inhibitor, regulates apoptosis in T. cruzi -infected cardiomyocytes and macrophages, impairing the cell death process (de Souza et al, 2008).…”

Section: Effect Of T Cruzi Infection In Cardiomyocyte Physiologymentioning

confidence: 99%

Current understanding of the Trypanosoma cruzi-cardiomyocyte interaction

Calvet¹,

Melo²,

Garzoni³

et al. 2012

Front. Immun.

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Trypanosoma cruzi, the etiological agent of Chagas disease, exhibits multiple strategies to ensure its establishment and persistence in the host. Although this parasite has the ability to infect different organs, heart impairment is the most frequent clinical manifestation of the disease. Advances in knowledge of T. cruzi–cardiomyocyte interactions have contributed to a better understanding of the biological events involved in the pathogenesis of Chagas disease. This brief review focuses on the current understanding of molecules involved in T. cruzi–cardiomyocyte recognition, the mechanism of invasion, and on the effect of intracellular development of T. cruzi on the structural organization and molecular response of the target cell.

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“…After 48 h induction with TMP-lactate the majority of amastigotes expressing these fusion proteins stained positive, indicating that apoptosis-like cell death in amastigotes occurred with the expression of all these proteins. It has been reported that T. cruzi could undergo apoptosis-like cell death [37,38]. However, the pathways leading to apoptosis-like cell death in this organism require further explorations.…”

Section: Discussionmentioning

confidence: 99%