Document Detail

Modulation of phagocytosis of apoptotic neutrophils by supernatant from dexamethasone-treated macrophages and annexin-derived peptide Ac(2-26).
MedLine Citation:
PMID:  15749912     Owner:  NLM     Status:  MEDLINE    
Phagocytic clearance of apoptotic leukocytes plays an important role in the resolution of inflammation. The glucocorticoid-inducible protein annexin 1 and annexin 1-derived peptides show potent anti-inflammatory responses in acute and chronic inflammation. In this study, we report that the annexin 1-derived peptide (Ac(2-26)) significantly stimulates nonphlogistic phagocytosis of apoptotic polymorphonuclear leukocytes (PMNs) by human monocyte-derived macrophages (Mphi). Peptide Ac(2-26)-stimulated phagocytosis is accompanied by rearrangement of the Mphi actin cytoskeleton. To investigate the potential role of endogenous annexin on clearance of apoptotic cells, Mphi were cultured for 5 days in the presence of dexamethasone. Supernatants collected from dexamethasone-treated Mphi significantly enhanced the ability of naive Mphi to engulf apoptotic PMNs. This effect was blocked by an annexin blocking Ab, by immunodepletion of the supernatants, and by the formyl peptide receptor/lipoxin receptor antagonist Boc1. In addition, we show that bone marrow-derived Mphi from annexin 1-null mice present a 40% decreased phagocytosis of apoptotic PMNs compared with cells taken from littermate controls. In conclusion, these results emphasize the pivotal role of annexin 1 as mediator for clearance of apoptotic cells and expand its potential therapeutic role in controlling inflammatory diseases.
Paola Maderna; Simon Yona; Mauro Perretti; Catherine Godson
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  174     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2005 Mar 
Date Detail:
Created Date:  2005-03-07     Completed Date:  2005-04-28     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3727-33     Citation Subset:  AIM; IM    
Department of Medicine and Therapeutics, The Conway Institute of Biomolecular and Biomedical Research, The Dublin Molecular Medicine Centre, University College Dublin, Dublin, Ireland.
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MeSH Terms
Actins / metabolism
Annexin A1 / deficiency,  genetics,  immunology,  pharmacology*
Cyclic AMP / metabolism
Cyclic AMP-Dependent Protein Kinases / metabolism
Dexamethasone / pharmacology
Interleukin-8 / biosynthesis
Macrophages / drug effects*,  immunology*,  metabolism
Mice, Knockout
Neutrophils / cytology*,  immunology*
Phagocytosis / drug effects
Transforming Growth Factor beta / biosynthesis
Reg. No./Substance:
0/Actins; 0/Annexin A1; 0/Interleukin-8; 0/Peptides; 0/Transforming Growth Factor beta; 0/annexin A1 peptide (2-26); 50-02-2/Dexamethasone; 60-92-4/Cyclic AMP; EC AMP-Dependent Protein Kinases

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