Respiratory burst activity of monocytes from patients with non-insulin-dependent diabetes mellitus.

Monocytes from patients with poorly controlled non-insulin-dependent diabetes mellitus (NIDDM) show a decrease in intracellular bactericidal function. To determine whether this reduced bactericidal function is mediated by an impaired oxygen-dependent mechanism, we assayed the production of superoxide (O2-) and hydrogen peroxide (H2O2) by monocytes from poorly controlled NIDDM patients (n = 12), well controlled NIDDM patients (n = 12) and healthy subjects (n = 16). Using phorbol myristate acetate (PMA) as stimulant, the production of O2- by fresh monocytes was significantly decreased in poorly controlled NIDDM patients (231 +/- 30 nmol/mg protein/2-h) as compared with that of well controlled NIDDM patients (430 +/- 81 nmol/mg protein/2-h) and that of healthy subjects (399 +/- 61 nmol/mg protein/2-h), respectively (P < 0.05). Using opsonized zymosan (OZ) as stimulant, the production of O2- by fresh monocytes was also notably decreased in patients with poorly controlled NIDDM (312 +/- 42 nmol/mg protein/2-h) as compared with that of patients with well controlled NIDDM (688 +/- 92 nmol/mg protein/2-h) and that of healthy subjects (539 +/- 96 nmol/mg protein/2-h), respectively (P < 0.05). Poorly controlled NIDDM patients had a significant decrease in the production of H2O2 by monocytes, either stimulated by PMA or OZ, as compared with that of well controlled NIDDM patients and that of healthy subjects, respectively (P < 0.05). Enhancement of the production of O2- and H2O2 occurred in healthy subjects (150% increase) as well as NIDDM patients (170% increase) after a preincubation of monocytes with interferon-gamma (IFN-gamma 100 U/ml) for 48 h. The respiratory burst activity of both fresh and cultured monocytes from well controlled NIDDM patients was not significantly different from that of healthy subjects. This study suggests that both, strict metabolic control and in vitro culture with IFN-gamma may improve the monocyte oxygen-dependent bactericidal mechanism in NIDDM patients.