Alveolar macrophage uptake of the environmental particulate titanium dioxide: role of surfactant components.

Pulmonary surfactant components can modulate uptake of microorganisms and viruses by alveolar macrophages (AMs), but little is known about their role in the uptake and clearance of inert environmental particulates. We tested the hypotheses that surfactant components [e.g., surfactant protein A (SpA) and the artificial bovine surfactant Survanta] modulate phagocytosis of inert environmental particulates by acting as particle opsonins, or by direct activation of AMs. AM uptake of a model inert particulate [titanium dioxide (TiO2)] was measured using flow cytometry to quantitate increased right angle scatter caused by particle uptake (e.g., fold increase in right angle scatter versus control: 2.6 +/- 0.3; and 5.0 +/- 0.2 for AMs plus TiO2, 20 and 80 micrograms/ml TiO2, respectively). Opsonization of TiO2 with surfactant components resulted in a modest increase in AM uptake compared with that of unopsonized TiO2 [e.g., fold increase, uptake of TiO2 (50 micrograms/ml), opsonized with SpA, Survanta, and rat immunoglobulin G, respectively: 1.6 +/- 0.1; 1.3 +/- 0.01; 1.5 + 0.02, n = 3-4]. Uptake of inert latex beads was similarly enhanced after opsonizing with SpA and Survanta (beads per cell: unopsonized, 3.2 +/- 0.40; SpA, 5.0 +/- 0.55; Survanta, 6.0 +/- 0.12; n = 3-6). Pretreating AMs with surfactant components and measuring the subsequent uptake of unopsonized TiO2 resulted in approximately the same magnitude of enhancement. The data indicate that surfactant components can increase AM phagocytosis of environmental particulates in vitro, but only slightly relative to the already avid AM uptake of unopsonized particles.