Inhibition of Fas-mediated apoptosis by Trypanosoma cruzi infection

Nakajima‐Shimada, Junko; Zou, Chunbin; Takagi, Motoki; Umeda, Masato; Nara, Takeshi; Aoki, Takashi

doi:10.1016/s0304-4165(00)00059-3

Cited by 43 publications

(41 citation statements)

References 34 publications

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“…1B). However, it may be that serum-starved Schwann cells would have continued to resist developing apoptosis if they were bearing a heavier intracellular parasitism, as suggested by recent results with Fas-induced apoptosis of T. cruzi-infected carcinoma and fibrosarcoma cells (24).…”

Section: T Cruzi Invasion Blocks Apoptosis Of Schwann Cellsmentioning

confidence: 98%

Trypanosoma cruzitrans-sialidase: A potent and specific survival factor for human Schwann cells by means of phosphatidylinositol 3-kinase/Akt signaling

Chuenkova

Furnari

Cavenee

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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Section: T Cruzi Invasion Blocks Apoptosis Of Schwann Cellsmentioning

confidence: 98%

Trypanosoma cruzitrans-sialidase: A potent and specific survival factor for human Schwann cells by means of phosphatidylinositol 3-kinase/Akt signaling

Chuenkova

Furnari

Cavenee

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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“…In this complex, procaspase-8 is activated to caspase-8, triggering the proteolytic cascade of effecter caspases leading to cell death . We previously demonstrated that induction of Fas-and TNFRmediated apoptosis was more strongly inhibited in T. cruziinfected cells than in uninfected cells and that caspase-8 activity could not be measured upon Fas stimulation of T. cruzi-infected cells (Nakajima-Shimada et al, 2000). We also showed that x-ray, H 2 O 2 , cholchicine, and etoposide, respectively, induced an essentially same degree of apoptosis between T. cruzi-infected and uninfected cells.…”

Section: Introductionmentioning

confidence: 86%

“…HT1080 cells (2 ϫ 10 5 ) were infected with 4 ϫ 10 5 T. cruzi trypomastigotes (Tulahuen strain) and cultured for 4 d. A cell population with an infection rate greater than 80% was considered as infected cells. The infection complex of HT1080 cells and T. cruzi was maintained as described (Nakajima-Shimada et al, 2000).…”

Section: Cells and Parasitesmentioning

confidence: 99%

“…After cultivation for 24 -30 h, the cells were infected with 2 ϫ 10 6 trypomastigotes as previously described (Nakajima-Shimada et al, 2000), incubated for 24 h further, and harvested for Western blotting or apoptosis induction followed by cell death assay.…”

Section: Sirna Experimentsmentioning

confidence: 99%

“…Because our previous study has demonstrated that caspase-8 activity could not be measured upon Fas stimulation of T. cruzi-infected cells (Nakajima-Shimada et al, 2000), expression of c-FLIP protein in T. cruzi-infected and uninfected cells was examined by Western blotting using an anti-c-FLIP antibody that recognizes both c-FLIP long (c-FLIP L ) and c-FLIP short (c-FLIP S ; Figure 1A). Both c-FLIP L and c-FLIP S , which are generated by alternative splicing, block procaspase-8 activation at the DISC and consequently inhibit death receptor-mediated apoptosis (Thome and Tschopp, 2001).…”

Section: T Cruzi Infection Up-regulates C-flip L Protein Expressionmentioning

confidence: 99%

See 2 more Smart Citations

Trypanosoma cruziPosttranscriptionally Up-Regulates and Exploits Cellular FLIP for Inhibition of Death-inducing Signal

Hashimoto

Nakajima‐Shimada

Aoki

2005

MBoC

Self Cite

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Toll-like receptor-2 and interleukin-6 mediate cardiomyocyte protection from apoptosis during Trypanosoma cruzi murine infection

Ponce

Cano

Silva

et al. 2011

Med Microbiol Immunol

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Local innate immunity plays a key role in initiating and coordinating homeostatic and defense responses in the heart. We have previously reported that the cardiotropic parasite Trypanosoma cruzi, the etiological agent of Chagas disease, protects cardiomyocytes against growth factor deprivation-induced apoptosis. In this study, we investigated cardiomyocyte innate immune response to T. cruzi infection and its role in cellular protection from apoptosis. We found that Toll-like receptor (TLR) 2-expressing cells were strongly increased by the parasite in BALB/c neonatal mouse cardiomyocyte cultures. Using a dominant-negative system, we showed that TLR2 mediated cardiomyocyte survival and the secretion of interleukin (IL) 6, which acted as an essential anti-apoptotic factor. Moreover, IL6 released by infected cells, as well as the recombinant bioactive cytokine, induced the phosphorylation of the signal transducers and activators of transcription-3 (STAT3) in cultured cardiomyocytes. In accord with the in vitro results, during the acute phase of the infection, TLR2 expression increased 2.9-fold and the anti-apoptotic factor Bcl-2 increased 4.5-fold in the cardiac tissue. We have clearly shown a cross-talk between the intrinsic innate response of cardiomyocytes and the pro-survival effect evoked by the parasite.

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Inhibition of Fas-mediated apoptosis by Trypanosoma cruzi infection

Cited by 43 publications

References 34 publications

Trypanosoma cruzitrans-sialidase: A potent and specific survival factor for human Schwann cells by means of phosphatidylinositol 3-kinase/Akt signaling

Trypanosoma cruzitrans-sialidase: A potent and specific survival factor for human Schwann cells by means of phosphatidylinositol 3-kinase/Akt signaling

Trypanosoma cruziPosttranscriptionally Up-Regulates and Exploits Cellular FLIP for Inhibition of Death-inducing Signal

Toll-like receptor-2 and interleukin-6 mediate cardiomyocyte protection from apoptosis during Trypanosoma cruzi murine infection

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