INCREASED OXYGEN SPECIES GENERATION IN BLOOD MONOCYTES OF ASTHMATIC-PATIENTS

Besides eosinophils, inflammatory processes In asthma are characterized by an infiltration of inflammatory cells, including mononuclear phagocytes, such as alveolar macrophages (AM) and blood monocytes, in the airways. Monocyte activation has been observed in the blood after exercise or allergen-induced asthma. Stimulated AM in chronic and stable asthmatic patients have been shown to release oxygen species. We thus investigated the intensity of the activation of monocytes from 18 asthmatic patients compared with 18 healthy subjects. Oxygen species release was analyzed for monocytes in suspension by chemiluminescence using a luminometer and for monocytes maintained in adherence using conventional assay and video imaging camera. Circulating blood monocytes in suspension from asthmatic patients and control subjects showed the same baseline free radical release. Monocytes in suspension from asthmatic patients were more stimulatable by PMA: specifically, monocytes release more H2O and peaks of O-2-radical-anion are sooner; moreover, peaks of total free radical release are higher, and this plateau is sustained. Compared with monocytes from control subjects, those from asthmatic patients evaluated after adherence show a higher baseline for O-2-radical-anion and higher total free radical release. Monocytes from asthmatic patients spontaneously release more O-2-radical-anion over time in nonstimulated cells and release more O-2-radical-anion with PMA stimulation; they show the same peak level total free radical release as those from control subjects after stimulation. SOD activity analysis on adherent monocytes was lower in asthmatic compared with control subjects. These data show that monocytes from asthmatic patients were activated compared with control monocytes. The difference between the suspension and adherence procedures indicated that monocyte margination and adherence on endothelial cells and bronchoalveolar walls could be associated with increased oxygen species release in asthma.