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Blood, Vol. 93 No. 2 (January 15), 1999:
pp. 674-685
Caspases Mediate Tumor Necrosis Factor- -Induced Neutrophil
Apoptosis and Downregulation of Reactive Oxygen Production
Kouhei Yamashita,
Atsushi Takahashi,
Susumu Kobayashi,
Hirokazu Hirata,
Peter W. Mesner Jr,
Scott H. Kaufmann,
Shin Yonehara,
Kokichi Yamamoto,
Takashi Uchiyama, and
Masataka Sasada
From the Department of Hematology and Oncology, Clinical Sciences for
Pathological Organs, Graduate School of Medicine, the Department of
Viral Oncology, Institute for Virus Research, and the College of
Medical Technology, Kyoto University, Kyoto, Japan; and the Division of
Oncology Research, Mayo Clinic, Rochester, MN.
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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