Role of an oxidative stress in the macrophage dysfunction caused by erythrophagocytosis

A phagocytic challenge with immunoglobulin G (IgG)-coated erythrocytes (EIg Gs) has been shown to cause a subsequent depression of macrophage respirato ry burst capacity and phagocytic function. The present study evaluated the hypothesis that this macrophage dysfunction is caused by an oxidative stres s. An oxidative stress induced by ferric ammonium citrate (FAC) plus cumene hydroperoxide (CHP) caused a depression of macrophage function that was at tenuated by antioxidants and iron chelators. In contrast, the same antioxid ants and iron chelators did not alter changes caused by a challenge with EI gGs. EIgG challenge caused an increase in lipid peroxidation but failed to deplete glutathione (GSH) or decrease the activity of glyceraldehyde-3-phos phate dehydrogenase (GA-3-PD), suggesting that there was only a slight oxid ative stress. Inhibition of the Fc gamma receptor (Fc gamma R) stimulated r espiratory burst by removing calcium during the challenge did not attenuate the changes caused by an EIgG challenge. A phagocytic challenge with noner ythrocyte particles, IgG-coated beads (BIgGs), did not depress the respirat ory burst capacity but did depress phagocytic function. Fc gamma R expressi on was depressed following a phagocytic challenge but not an oxidative stre ss. Thus, an oxidative stress can depress macrophage function, but the dysf unction caused by a phagocytic challenge with EIgGs involves Fc gamma R dep letion and the erythrocyte contents rather than an oxidative stress. (C) 19 99 Elsevier Science Inc.