scholarly journals Synthetic immunostimulatory glycans interference with host cell apoptosis upon of Toxoplasma gondii infection, in vitro

2017 ◽  
Vol 31 (1) ◽  
pp. 43-49
Author(s):  
S.H. Eassa
2000 ◽  
Vol 86 (5) ◽  
pp. 922
Author(s):  
Giovanni Widmer ◽  
Elizabeth A. Corey ◽  
Barry Stein ◽  
Jeffrey K. Griffiths ◽  
Saul Tzipori

2008 ◽  
Vol 118 (3) ◽  
pp. 331-337 ◽  
Author(s):  
E.M. De Souza ◽  
M. Meuser-Batista ◽  
D.G. Batista ◽  
B.B. Duarte ◽  
T.C. Araújo-Jorge ◽  
...  

Gene ◽  
2018 ◽  
Vol 649 ◽  
pp. 93-98 ◽  
Author(s):  
Jia Guo ◽  
Mengjiao Zhou ◽  
Xin Liu ◽  
Yunzhi Pan ◽  
Runjun Yang ◽  
...  

2001 ◽  
Vol 52 (Supplement) ◽  
pp. 102
Author(s):  
Junko SHIMADA ◽  
Chunbin ZOU ◽  
Takeshi NARA ◽  
Miriam PONSTAN ◽  
Takashi AOKI ◽  
...  

2001 ◽  
Vol 114 (19) ◽  
pp. 3495-3505
Author(s):  
Stefan Goebel ◽  
Uwe Gross ◽  
Carsten G. K. Lüder

The obligate intracellular protozoan parasite Toxoplasma gondii has been shown to protect different cell types from apoptosis induced by a variety of pro-apoptotic treatments. However, the precise cell biological mechanisms of this inhibition remained unknown. As shown in this study, apoptosis in human-derived HL-60 and U937 cells induced by treatment with actinomycin D or TNF-α in combination with cycloheximide, respectively, was indeed dose-dependently downregulated by prior infection with T. gondii, as determined by DNA fragmentation assays. Cleavage of caspase 3 and caspase 9 after treatment with pro-apoptotic stimuli was considerably diminished by T. gondii. Furthermore, release of mitochondrial cytochrome c during apoptosis in HL-60 cells was prevented by intracellular parasites and this was correlated with the absence of DNA strand breaks on the single cell level. Inhibition of cytochrome c release coincided with a twofold upregulation of Mcl-1 protein levels in HL-60 and U937 cells, while Bcl-2 expression did not increase after infection. Parasitic interference with the caspase cascade led to a reduced proteolytic cleavage of the nuclear target molecule protein kinase Cδ. In parallel, poly(ADP-ribose) polymerase protein levels were prominently downregulated by T. gondii, irrespective of whether HL-60 and U937 cells had been treated with pro-apototic stimuli or left untreated. However, poly(ADP-ribose) polymerase mRNA levels remained unchanged after infection as determined by RT-PCR analyses. These observations suggest that T. gondii has evolved different mechanisms that may contribute to downregulation of host cell apoptosis, namely inhibition of cytochrome c release and subsequent caspase activation as well as downregulation of poly(ADP-ribose) polymerase protein levels.


2013 ◽  
Vol 133 (4) ◽  
pp. 462-471 ◽  
Author(s):  
Juan-Hua Quan ◽  
Guang-Ho Cha ◽  
Wei Zhou ◽  
Jia-Qi Chu ◽  
Yoshifumi Nishikawa ◽  
...  

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