Part of the Methods in Molecular Medicine™ book series (MIMM, volume 78)
Detection of Reactive Oxygen Intermediate Production by Macrophages
The reparative phenomena that follow sterile tissue injury are an ordered sequence of partially overlapping events and include the macrophage as a key cell type in orchestrating the process of repair. Several studies suggest that the wound-derived macrophage acquires a functional phenotype that is congruent with its specialized role in repair, and that this phenotype is determined by factors within the wound milieu. This phenotype distinguishes the wound macrophages from macrophages obtained at other anatomical sites. Evidence in support of this hypothesis includes the findings that wound-derived macrophages are more phagocytic and fungicidal than resident or immuneelicited peritoneal macrophages (1). Wound macrophages demonstrate a substantially greater capacity to suppress splenocyte proliferation in a nitric oxide (NO)—dependent mechanism but fail to kill NO-sensitive tumor cells that readily succumb to immune activated cells (2,3). Wound macrophages also demonstrate differential responsiveness to activation signals. Exposure of wound macrophages to anoxia results in an increase in arginase activity not seen by similar exposure of immune-elicited or resident peritoneal cells (4). Wound macrophages are deficit in their capacity to generate reactive oxygen intermediates (ROIs) even when challenged with classic activators of the respiratory burst oxidase system (Fig. 1 Fig. 2 Fig. 3 4) (5). Several assays for measuring ROI production in inflammatory cells are provided in this chapter.
KeywordsNADPH Oxidase Activity Arginase Activity Reactive Oxygen Intermediate Sodium Dithionite Superoxide Release
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
© Humana Press Inc., Totowa, NJ 2003