Autor: |
Nessel CC; Department of Surgery, Rhode Island Hospital and Brown University, Providence, Rhode Island 02903, USA., Henry WL Jr, Mastrofrancesco B, Reichner JS, Albina JE |
Jazyk: |
angličtina |
Zdroj: |
The American journal of physiology [Am J Physiol] 1999 Jun; Vol. 276 (6), pp. R1587-94. |
DOI: |
10.1152/ajpregu.1999.276.6.R1587 |
Abstrakt: |
Macrophages from experimental wounds in rats were tested for their capacity to generate reactive oxygen intermediates. Measurements of superoxide and H2O2 release, O-2-dependent lucigenin chemiluminescence, oxygen consumption, hexose monophosphate shunt flux, and NADPH oxidase activity in cell lysates indicated, at best, the presence of a vestigial respiratory burst response in these cells. The inability of wound cells to release O-2 was not rekindled by priming with endotoxin or interferon-gamma in vivo or in vitro. NADPH oxidase activity in a cell-free system demonstrated that wound macrophage membranes, but not their cytosols, were capable of sustaining maximal rates of O-2 production when mixed with their corresponding counterparts from human neutrophils. Immune detection experiments showed wound macrophages to be particularly deficient in the cytosolic component of the NADPH oxidase p47-phox. Addition of recombinant p47-phox to the human neutrophil-cell membrane/wound macrophage cytosol cell-free oxidase assay, however, failed to support O-2 production. Present findings indicate an unexpected deficit of wound macrophages in their capacity to generate reactive oxygen intermediates. |
Databáze: |
MEDLINE |
Externí odkaz: |
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