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The data presented here suggest that SP-A and SP-D perform distinct, as well as complementary, host defense functions in the lung. Although both proteins are agglutinins, opsonins, and inflammatory immunomodulators, they interact uniquely with various pathogens and inflammatory cells. For instance, SP-A and SP-D appear to have opposite effects on the phagocytosis of Mycobacterium tuberculosis and on regulation of oxidant responses from alveolar macrophages. The pulmonary collectins partition into different microdomains within the airway lining; SP-D appears to prefer the aqueous phase of the ALL but may be weakly associated with the surface of epithelial cells, whereas SP-A is enriched in tubular myelin and at surfactant membrane interfaces. While the initial view held that tubular myelin would be required for surfactant regulation and function, it now appears more likely that it serves a primary host defense role as a solid-phase, high-density SP-A array that optimizes the surface properties of surfactant and the interception of inhaled microbes at the air-lung interface.

The pulmonary collectins, SP-A and SP-D, orchestrate innate immunity in the lung