The objective of the present study was to test the effect of platelet-activating factor (PAF) on rat alveolar macrophages. PAF alone did not simulate superoxide secretion from alveolar macrophages. However, PAF (10^-5M) significantly enhanced phagocyt...
The objective of the present study was to test the effect of platelet-activating factor (PAF) on rat alveolar macrophages. PAF alone did not simulate superoxide secretion from alveolar macrophages. However, PAF (10^-5M) significantly enhanced phagocytic activator zymosan-induced superoxide secretion from alveolar macrophages. This enhancement of PAF plus zymosan was 30% above the sum of the separate effects of PAF and zymosan. Similarly, PAF (1.3×10^-5M) was not a direct stimulant of alveolar macrophages, as it had no stimulatory effect on chemiluminescence generation, but potentiated zymosan-induced activation of chemiluminescence, i.e., 162% above the separate effects of each stimulant. PAF (10^-16~10^-6M) also failed to stimulate IL-1 production from alveolar macrophages. In contrast, when both PAF (10^-10M) and lipopolysaccharide(LPS) (1㎍/㎖) were added together at the initiation of the culture, IL-1 production by alveolar macrophages. Collectively, these data suggest that PAF alone does not activate the release of bioactive products from alveolar macrophages. However, PAF appears to act as a priming mediator that potentiates stimuli-induced macrophage activity. These novel actions of PAF prove its role as a potent mediator of inflammatory and immune responses in the lung.