| Involvement of caspases and of mitochondria in Fas ligation-induced eosinophil apoptosis: modulation by interleukin-5 and interferon-gamma. | |
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MedLine Citation:
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PMID: 11698497 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In this study, we examined the relative importance of caspases and mitochondria in Fas-mediated eosinophil apoptosis. Stimulation of human peripheral blood eosinophils with an agonistic anti-human Fas monoclonal antibody, but not with control IgM, induced a time-dependent increase in their apoptosis, which was associated with a loss in mitochondrial transmembrane potential (DeltaPsi(m)) and with caspase-8 and caspase-3 activation. Interleukin (IL)-5 and interferon (IFN)-gamma, two cytokines known to prolong eosinophil survival, inhibited Fas-mediated apoptosis and caspase activation but poorly affected the decrease in DeltaPsi(m). Eosinophil incubation with bongkrekic acid, an inhibitor of the mitochondrial permeability transition pore (MPTP) opening, failed to modify Fas-mediated loss in DeltaPsi(m), caspase activation, and apoptosis. In contrast, caspase inhibitors markedly reduced eosinophil apoptosis without significantly affecting DeltaPsi(m) dissipation. We conclude that caspase-8 and caspase-3 activation, but not MPTP opening, mediate Fas-induced eosinophil apoptosis and are the main targets for the protective effect of IL-5 and IFN-gamma. |
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Authors:
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S Létuvé; A Druilhe; M Grandsaigne; M Aubier; M Pretolani |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of leukocyte biology Volume: 70 ISSN: 0741-5400 ISO Abbreviation: J. Leukoc. Biol. Publication Date: 2001 Nov |
Date Detail:
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Created Date: 2001-11-07 Completed Date: 2001-12-07 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8405628 Medline TA: J Leukoc Biol Country: United States |
Other Details:
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Languages: eng Pagination: 767-75 Citation Subset: IM |
Affiliation:
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Institut National de la Santé et de la Recherche Médicale U408, Faculté de Médecine Xavier Bichat, Hôpital Bichat, Paris, France. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Amino Acid Chloromethyl Ketones
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pharmacology Animals Antibodies, Monoclonal / pharmacology Antigens, CD95 / immunology, physiology* Apoptosis / drug effects* Bongkrekic Acid / pharmacology Caspase 3 Caspase 8 Caspase 9 Caspases / antagonists & inhibitors, physiology* Cysteine Proteinase Inhibitors / pharmacology Cytochrome c Group / metabolism Eosinophils / cytology, drug effects*, enzymology, ultrastructure Fas Ligand Protein Humans Hypereosinophilic Syndrome / blood Immunoglobulin M / pharmacology Interferon-gamma, Recombinant / pharmacology* Interleukin-5 / pharmacology* Intracellular Membranes / drug effects, physiology Ion Channels* Membrane Glycoproteins / physiology* Membrane Potentials / drug effects Membrane Proteins / antagonists & inhibitors, physiology Mice Mitochondria / drug effects, physiology* Mitochondrial Membrane Transport Proteins Oligopeptides / pharmacology Pulmonary Eosinophilia / immunology, pathology Recombinant Proteins / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Amino Acid Chloromethyl Ketones; 0/Antibodies, Monoclonal; 0/Antigens, CD95; 0/Cysteine Proteinase Inhibitors; 0/Cytochrome c Group; 0/FASLG protein, human; 0/Fas Ligand Protein; 0/Fasl protein, mouse; 0/Immunoglobulin M; 0/Interferon-gamma, Recombinant; 0/Interleukin-5; 0/Ion Channels; 0/Membrane Glycoproteins; 0/Membrane Proteins; 0/Mitochondrial Membrane Transport Proteins; 0/Oligopeptides; 0/Recombinant Proteins; 0/benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone; 0/benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone; 0/benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 0/mitochondrial permeability transition pore; 11076-19-0/Bongkrekic Acid; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/CASP8 protein, human; EC 3.4.22.-/CASP9 protein, human; EC 3.4.22.-/Casp3 protein, mouse; EC 3.4.22.-/Casp8 protein, mouse; EC 3.4.22.-/Casp9 protein, mouse; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 8; EC 3.4.22.-/Caspase 9; EC 3.4.22.-/Caspases |
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