|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
5
|
|
pubmed:dateCreated |
2004-4-22
|
|
pubmed:abstractText |
Human peripheral blood monocytes become apoptotic following phagocytosis and killing of Staphylococcus aureus. Although this type of monocyte apoptosis is known to be initiated by Fas-Fas ligand (FasL) interactions, the downstream signaling pathway has not been determined. In this work the involvement of mitochondria and the kinetics of caspase-8 and caspase-3 activation after phagocytosis of S. aureus were studied. Caspase-8 activity was measured in cell lysates by using the fluorogenic substrate Ac-IETD-AFC. Active caspase-3 levels and mitochondrial membrane potential (Deltapsi(m)) were measured in whole cells by flow cytometry using monoclonal antibodies reacting with activated caspase-3 and chloromethyl-X-rosamine, respectively. The results show that caspase-8 was activated shortly after phagocytosis of bacteria. Caspase-8 activation was followed by progressive disruption of Deltapsi(m), which is associated with the production of reactive oxygen intermediates. The irreversible caspase-8 inhibitor zIETD-FMK prevented the disruption of Deltapsi(m) and the release of cytochrome c from S. aureus-exposed monocytes. Caspase-3 activation occurred following disruption of Deltapsi(m). These results strongly suggest that apoptosis of monocytes that have phagocytosed and killed S. aureus is driven by the Fas-FasL-initiated pathway, which is typical for type II cells.
|
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-10417194,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-10547689,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-10769002,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-10802163,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-10839799,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-10932094,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-11034400,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-11137044,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-11179290,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-11517432,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-11520805,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-11696559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-11731108,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-12218135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-12515825,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-12729581,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-12894214,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-12969378,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-13678697,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-2538546,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-3623696,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-3781627,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-7722446,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-8018341,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-8132337,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-8926095,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-8946140,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-9064332,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-9206994,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-9353266,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-9423876,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-9501089,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-9525905,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-9721089,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-9727492,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15102767-9878531
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
May
|
|
pubmed:issn |
0019-9567
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
72
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
2590-7
|
|
pubmed:dateRevised |
2009-11-18
|
|
pubmed:meshHeading |
pubmed-meshheading:15102767-Apoptosis,
pubmed-meshheading:15102767-Caspase 3,
pubmed-meshheading:15102767-Caspase 8,
pubmed-meshheading:15102767-Caspases,
pubmed-meshheading:15102767-Enzyme Activation,
pubmed-meshheading:15102767-Humans,
pubmed-meshheading:15102767-Immunity, Innate,
pubmed-meshheading:15102767-Membrane Potentials,
pubmed-meshheading:15102767-Mitochondria,
pubmed-meshheading:15102767-Monocytes,
pubmed-meshheading:15102767-Phagocytosis,
pubmed-meshheading:15102767-Reactive Oxygen Species,
pubmed-meshheading:15102767-Staphylococcus aureus
|
|
pubmed:year |
2004
|
|
pubmed:articleTitle |
Caspase-8 activation precedes alterations of mitochondrial membrane potential during monocyte apoptosis induced by phagocytosis and killing of Staphylococcus aureus.
|
|
pubmed:affiliation |
Department of Immunology, Faculty of Biotechnology, Jagiellonian University, Cracow, Poland.
|
|
pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
|
