Научно-практический журнал
[About us] Journal 'Cytokines & Inflammation'

197376, Санкт-Петербург, ул. Акад. Павлова, д. 12,
Институт экспериментальной медицины РАМН
Тел.: (812) 543 52 14, +7 921 984 11 30, +7 921 909 55 49
Факс: (812) 543 52 14
Web: cytokines.ru


Year 2010
Number 1 Number 2
Number 3 Number 4

About journal



Rules for authors

Contact us


Site map

Our partners:


Русский языкEnglish language
Site map Contact us

Contents | Next article | Previous article

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

Subscribe for 2011 year

Order PDF of this article

Original Articles

Number 1'2003


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.

Contents | Next article | Previous article

© 2007 Cytokines and inflammation