Acceleration of Human Neutrophil Apoptosis by Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)

2003 ◽  
Vol 104 (s49) ◽  
pp. 58P-58P
Author(s):  
Stephen A. Renshaw ◽  
Jasvir S Parmar ◽  
Vanessa Singleton ◽  
Sarah J. Rowe ◽  
Steven K. Dower ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Human Neutrophil ◽  
Tumor Necrosis ◽  
Neutrophil Apoptosis ◽  
Necrosis Factor

In vitro effect of recombinant human tumor necrosis factor-α on canine neutrophil apoptosis

2006 ◽  
Vol 80 (2) ◽  
pp. 162-166 ◽  
Author(s):  
Keisuke Oguma ◽  
Junichi Sano ◽  
Rui Kano ◽  
Toshihiro Watari ◽  
Atsuhiko Hasegawa
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Human Tumor ◽  
Neutrophil Apoptosis ◽  
Human Tumor Necrosis Factor ◽  
Factor Α ◽  
Vitro Effect ◽  
Necrosis Factor

scholarly journals Inhibition of tumor necrosis factor-a induced neutrophil apoptosis by cyclic AMP : involvement of caspase cascade

2000 ◽  
Vol 82 ◽  
pp. 271
Author(s):  
Masayuki Niwa ◽  
Yutaka Kanamori ◽  
Hiroyuki Matsuno ◽  
Osamu Kozawa ◽  
Toshihiko Uematsu
Keyword(s):  
Tumor Necrosis Factor ◽  
Cyclic Amp ◽  
Tumor Necrosis ◽  
Neutrophil Apoptosis ◽  
Caspase Cascade ◽  
Necrosis Factor

Caspases Mediate Tumor Necrosis Factor-–Induced Neutrophil Apoptosis and Downregulation of Reactive Oxygen Production

Blood ◽  
1999 ◽  
Vol 93 (2) ◽  
pp. 674-685 ◽  
Author(s):  
Kouhei Yamashita ◽  
Atsushi Takahashi ◽  
Susumu Kobayashi ◽  
Hirokazu Hirata ◽  
Peter W. Mesner ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Caspase 8 ◽  
Neutrophil Apoptosis ◽  
Oxygen Production ◽  
Caspase Activation ◽  
Necrosis Factor ◽  
Superoxide Release

Tumor necrosis factor- (TNF-) exerts two separate effects on neutrophils, stimulating effector functions while simultaneously inducing apoptosis. We examined here the involvement of caspases in neutrophil apoptosis and the effect of TNF-–induced apoptosis on reactive oxygen production. Immunoblotting and affinity labeling showed activation of caspase-8, caspase-3, and a caspase with a large subunit of 18 kD (T18) in TNF-–treated neutrophils. Active caspase-6 and -7 were not detectable in this cell type. Caspase-8 activated caspase-3 and T18 in neutrophil cytoplasmic extracts. zVAD-fmk blocked neutrophil apoptosis, in parallel with the inhibition of caspase activation. TNF-–induced caspase activation was accompanied by a decrease in the ability of neutrophils to release superoxide anion. Conversely, TNF- treatment in the presence of zVAD-fmk caused a prolonged augmentation of superoxide release. Granulocyte-macrophage colony-stimulating factor inhibited TNF-–induced caspase activation and apoptosis, while reversing the diminution in superoxide release. These observations not only suggest that a caspase cascade mediates apoptotic events and downregulates oxygen radical production in TNF-–treated neutrophils, but also raise the possibility that suppression of caspase activation with enhanced proinflammatory actions of TNF- may underlie the pathogenesis of inflammatory diseases.

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