It has become increasingly evident that
pulmonary surfactant proteins, SP-A and
SP-D, present in the alveolar and bronchial epithelial fluid linings, not only play significant functions in the innate defense mechanism against pathogens, but also are involved in immunomodulatory roles, which result in the protection against, and resolution of,
allergen-induced airway
inflammation. Studies on
allergen-sensitized murine models, and asthmatic patients, show that SP-A and
SP-D can: specifically bind to aero-
allergens; inhibit mast cell degranulation and histamine release; and modulate the activation of alveolar macrophages and dendritic cells during the acute hypersensitive phase of allergic response. They also can alleviate chronic allergic
inflammation by inhibiting T-lymphocyte proliferation as well as increasing phagocytosis of
DNA fragments and clearance of apoptotic cell debris. Furthermore, it has emerged, from the studies on
SP-D-deficient mice, that, when these mice are challenged with
allergen, they develop increased eosinophil infiltration, and abnormal activation of lymphocytes, leading to the production of Th2
cytokines.
Intranasal administration of
SP-D significantly attenuated the asthmatic-like symptoms seen in
allergen-sensitized wild-type, and
SP-D-deficient, mice. These important findings provide a new insight of the role that
surfactant proteins play in handling environmental stimuli and in their immunoregulation of airway inflammatory disease.