Abstract
The resolution of inflammation is dependent on recognition and phagocytic removal of apoptotic cells by macrophages. Receptors for
apoptotic cells are sensitive to degradation by human neutrophil
elastase (HNE). We show in the present study that HNE cleaves
macrophage cell surface CD14 and in so doing, reduces phagocytic
recognition of apoptotic lymphocytic cells (Mutu 1). Using an improved
method of adenovirus-mediated transfection of macrophages with the HNE
inbibitor elafin, we demonstrate that elafin overexpression prevents
CD14 cleavage and restores apoptotic cell recognition by macrophages.
This approach of genetic modification of macrophages could be used to
restore apoptotic cell recognition in inflammatory conditions. (C) 2004
Federation of European Biochemical Societies. Published by Elsevier
B.V. All rights reserved.
Original language | English |
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Pages (from-to) | 80-84 |
Number of pages | 5 |
Journal | FEBS Letters |
Volume | 574 |
Issue number | 1-3 |
Early online date | 14 Aug 2004 |
DOIs | |
Publication status | Published - 10 Sept 2004 |
Keywords
- neutrophil elastase
- elafin
- macrophage
- apoptosis
- adenovirus
- gene therapy