Exercise enhances surfactant-mediated phagocytosis in bronchoalveolar macrophages

Severe exercise augments the phagocytic capability of bronchoalveolar macrophages (BAMs) in the absence of pulmonary surfactant, a lung immunity modulator in vivo. This study was to investigate whether the exercise effect on BAM phagocytosis is partially mediated by surfactant components. Male BALB/c mice (9-12 wk old) were divided into control and severe exercise groups. Mice in the exercise group received progressive treadmill running exercise until exhaustion. BAMs and lung lavage supernatant were collected under either sedentary or post-severe exercise conditions. Phagocytosis of IgG/C'-opsonized beads by BAMs was determined in the presence of lavage supernatant. Mannose, a monosaccharide competitor for the carbohydrate recognition domain of surfactant protein A (SP-A), and SP-A antibodies were applied to examine the role of SP-A in the exercise-induced facilitating effects on BAM phagocytosis. BAMs from either control or post-exercise animals had elevated phagocytosis of IgG/C'-opsonized beads when incubated with autologous lung lavage supernatant. The supernatant-mediated increase in BAM phagocytosis of IgG/C'-opsonized beads was dose-dependently inhibited by mannose or SP-A antibodies. In addition, higher concentrations of SP-A inhibitors were needed to inhibit BAM phagocytosis in post-exercise group than that in the control group. We also observed that SP-A inhibitors were ineffective in the absence of lung lavage supernatant. Furthermore, post-exercise, but not control, BAMs displayed time-dependent alterations in their membrane-bound SP-A amount during 30-min incubation with autologous lung lavage supernatant. SP-A plays a major role in the severe exercise-enhanced surfactant-mediated BAM phagocytosis.