DEFECTIVE OXIDATIVE METABOLIC RESPONSES INVITRO OF ALVEOLAR MACROPHAGES IN CHRONIC GRANULOMATOUS-DISEASE

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Abstract
After stimulation with bacteria, alveolar macrophages (AM) from uninfected normal subjects or persons with pneumonia approximately doubled their rates of O2 consumption, superoxide anion generation and glucose (1-14C) oxidation. Bacteria-stimulated AM from a patient with chronic granulomatous disease (CGD) failed to consume more O2, make superoxide anion or oxidize glucose. AM from the patient with CGD did not respond to stimulation by a chemical agent, phorbol myristate acetate, which increased the metabolic activities of AM from control subjects. The appearance, esterase and Gomori acid phosphatase staining, phagocytic ability, unstimulated O2 consumption and response to methylene blue of AM from the CGD patient were normal. The biochemical defect in patients with CGD is extended beyond abnormalities in their circulating neutrophils and monocytes, to their tissue-associated lung macrophages. AM from patients with CGD may have an additional abnormality in metabolism, i.e., a lack of enhanced mitochondrial respiration during phagocytosis. The selective action of phorbol myristate acetate, which stimulated the metabolic activities of normal AM, but not of those from the patient with CGD, was documented.

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