Chronic granulomatous disease (CGD) is characterized by severe, recurrent infections with bacteria and fungi, caused by a defect in the superoxide anion-producing NADPH-oxidase in polymorphonuclear (PMN) neutrophils. Treatment with interferon-gamma (IFN-γ) is associated with decreased frequency and severity of infections in CGD but the mechanism is unknown.

Objective of study: Since the inducible NO-synthase (iNOS) can be amplified by IFN-γ in e.g. murine macrophages, we hypothesized that IFN-γ might modulate nitric oxide (NO) release from CGD PMN.

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