Document Detail


Bid activation during induction of extrinsic and intrinsic apoptosis in eosinophils.
MedLine Citation:
PMID:  17549073     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Eosinophils readily undergo apoptosis when removed from a physiological environment via activation of the intrinsic cell death pathway. This can be further enhanced by certain chemicals (for example, glucocorticoid), or by extrinsic means (that is, Fas receptor engagement). In this investigation, we examined the relative importance of these pathways in cultured human peripheral blood eosinophils in the context of expression and activation of the BH3-only Bcl2 homologue Bid. Bid activation was examined under conditions where programmed cell death was either stimulated (via Fas engagement or glucocorticoid treatment) or inhibited (interleukin-5 (IL-5)) relative to control. Full-length Bid was found to be highly expressed in eosinophils, and processed to a similar extent during either agonist anti-Fas or glucocorticoid treatment. IL-5 blocked intrinsic Bid activation during factor withdrawal or glucocorticoid treatment, and partially attenuated that caused by Fas activation. Caspase 8 (but not caspase 9) antagonism partly but significantly affected receptor-mediated Bid activation and cell death; these processes were not altered by either caspase inhibitor during simple factor withdrawal or glucocorticoid treatment. Bid processing appears to be central to both intrinsic and extrinsic pathways of cell death in eosinophils. The role of IL-5 in blocking the intrinsic pathway of eosinophil apoptosis is underscored. Results of specific inhibition support the existence of Bid activation pathways in eosinophils other than those mediated by the classic initiator caspases.
Authors:
Manav Segal; Sultan Niazi; Michael P Simons; Steven A Galati; James G Zangrilli
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2007-06-05
Journal Detail:
Title:  Immunology and cell biology     Volume:  85     ISSN:  0818-9641     ISO Abbreviation:  Immunol. Cell Biol.     Publication Date:  2007 Oct 
Date Detail:
Created Date:  2007-10-04     Completed Date:  2008-01-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8706300     Medline TA:  Immunol Cell Biol     Country:  Australia    
Other Details:
Languages:  eng     Pagination:  518-24     Citation Subset:  IM    
Affiliation:
Department of Medicine, Division of Pulmonary and Critical Care Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis* / drug effects,  immunology
BH3 Interacting Domain Death Agonist Protein / metabolism*
Caspases, Initiator / antagonists & inhibitors
Cell Survival
Cells, Cultured
Eosinophils / metabolism,  physiology*
Humans
Interleukin-5 / pharmacology
Protease Inhibitors / pharmacology
Protein Processing, Post-Translational / drug effects
Signal Transduction / drug effects
Grant Support
ID/Acronym/Agency:
HL076646/HL/NHLBI NIH HHS; K08HL03663/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/BH3 Interacting Domain Death Agonist Protein; 0/BID protein, human; 0/Interleukin-5; 0/Protease Inhibitors; EC 3.4.22.-/Caspases, Initiator

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