Pulmonary surfactant and alveolar type II epithelial cells play important roles in lung defense mechanisms. We reported that native surfactant and its components (SP-A and phospholipid liposomes) as well as artificial surfactant (Surfactant-TA, S-TA) inhibited adherence, chemotaxis, release of superoxides and elastase of human peripheral neutrophils. Neutrophils reacted with S-TA showed characteristics of apoptotic cells. We also demonstrated that S-TA inhibited proliferation of rat lung fibroblasts and that S-TA protected a type II cell monolayer and enhanced its surfactant metabolism.
Surfactant replacement therapy significantly decreases a mortality of ARDS patients. Surfactant may improve gas exchanges by preventing alveolar collapse. We showed that superoxide production from neutrophils obtained from the hamster lungs, in which S-TA was instilled 24 hours after bleomycin administration, was significantly inhibited, compared to neutrophils from control animals. The rats, which were replaced with S-TA twenty four hours and seven days after receiving bleomycin administration, showed a decrease in lung collagen content, compared to control animals. These findings suggest that S-TA may inhibit neutrophil activation or fibroblast proliferation and may protect type II cells from their damage.
In summary, pulmonary surfactant was shown to have significant effects on functions of inflammatory cells, such as alveolar macrophages, lymphocytes, or neutrophils, as well as on those of stroma cells, such as fibroblasts or type II cells. Surfactant, together with type II celles, may be involved in the development of some kinds of pulmonary diseases. In the future aspects, development of new kinds of artificical surfactant as a therapeutic tool may be required, along with the studies on clinical usefulness and its mechanisms.