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Journal 'Cytokines & inflammation', 2003, No. 1

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Original Articles

Number 1'2003

CASPASE-INDEPENDENT CELL DEATH IN HUMAN NEUTROPHILS INDUCED BY TNFA

N.A. Maianski, D. Roos, T.W. Kuijpers

Objectives: To study mechanisms of TNFa-induced neutrophil cell death. Materials and Methods: Human neutrophil cell death induced by TNFa in the presence or absence of general caspase inhibitor zVAD-fmk and several antioxidants was studied by means of Annexin-V/PI staining and morphological examination of the cytospin preparations. Activation of caspase-8 and -3 was monitored by Western blotting, DNA laddering was investigated by agarose gel electrophoresis, mitochondria and Bax protein were analyzed by confocal microscopy. Neutrophil-derived cytoplast were prepared by discontinuos gradient ultracentrifugation. Results: TNFa alone induced apoptotic cell death in neutrophils within 6 hours of culturing with characteristic apoptotic features, which coincided with activation of caspase-8 and -3. However, when caspases were inhibited by zVAD-fmk, stimulation with TNFa still caused neutrophil cell death. This type of cell death lacked nuclear features of apoptosis and demonstrated no Bax redistribution, but did show mitochondria clustering and plasma membrane changes. Experiments with a scavenger of reactive oxygen species (ROS) and with an inhibitor of mitochondrial respiration and with neutrophil-derived cytoplasts (which lack mitochondria) indicated that TNFa + zVAD-fmk-induced cell death depends on mitochondria-derived ROS. Conclusion: TNFa can induce a "classical" caspase-dependent apoptosis and a "non-classical" caspase-independent cell death in human neutrophils.

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