A recombinant fragment of human surfactant protein D lacking the short collagen-like stalk fails to correct morphological alterations in lungs of SP-D deficient mice.

Emphysema-like pathology is a characteristic feature of surfactant protein D (SP-D) knock-out mice. Treatment with a recombinant fragment of human SP-D consisting of a short collagen-like stalk (but not the entire collagen-like domain of native SP-D), neck, and carbohydrate recognizing domain (CRD) inhibits development of emphysema-like pathology in SP-D deficient mice. On the other hand, it has been shown that the entire collagen-like domain is necessary for preventing SP-D knock-out mice from pulmonary emphysema development. Thus, in the present study, we aimed to elucidate the role of the short collagen-like stalk for the function of the recombinant fragment of human SP-D. We treated SP-D knock-out mice with a fragment of human SP-D lacking the short collagen-like stalk and compared the effects on lung morphology with results from untreated wild-type and SP-D knock-out mice and from SP-D knock-out mice treated with a recombinant fragment of human SP-D including the short collagen-like stalk. The fragment of SP-D lacking the short collagen-like stalk failed to correct pulmonary emphysematous alterations demonstrating the importance of the short collagen-like stalk for the biological activity of the recombinant fragment of human SP-D.