REGULATION OF THE RELEASE OF ALVEOLAR MACROPHAGE-DERIVED NEUTROPHIL CHEMOTACTIC FACTOR

Abstract

To further clarify the physiological role of the neutrophil-directed chemotactic factor derived from alveolar macrophages, those stimuli that regulate the quantity and kinetics of its release were evaluated in vitro. In short- term culture, particulate stimuli (Staphylococcus albus [S. aureus], Micropolyspora faeni, zymosan and Sepharose 4B) and IgG-immune complexes induced normal guinea pig alveolar macrophages to release significant quantities of this chemotactic factor. Serum opsonization of particulate stimuli resulted in significant augmentation of release of the chemotactic factor from alveolar macrophages responding to these particles. This serum augmentation was associated with the fixation of C3b [b fragment of complement component 3] to the particle surface via the alternative C pathway. Purified C3b by itself was also capable of inducing release of this macrophage-derived mediator. Partial characterization of this chemotactic factor revealed that it was a material of low MW (400-600 daltons), and that it was antigenically and physically distinct from C5a. The induction of chemotactic factor release from alveolar macrophages responding to microorganisms, noninfectious particulates, antigen-complexed IgG and C3b may contribute to the pathophysiologic events observed in those lung diseases characterized by an influx of neutrophils into the pulmonary parenchyma.