In the lung, under normal conditions, microorganisms at first encounter components of the innate immune response, particularly alveolar macrophages, dendritic cells and the lung collectins, the surfactant protein (SP)-A1, -A2 and -D. SP-A1, -A2 and -D belong to the collectin subgroup of the C-type lectin superfamily, and contain both collagen-like and carbohydrate-binding recognition domains (CRDs) [4] . Upon binding to pathogen-associated molecular patterns (PAMPs), SP-A and SP-D enhance the opsonophagocytosis of common respiratory pathogens by macrophages [5, 6] . Mice rendered SP-A or SP-D deficient exhibit increased susceptibility to several bacteria and viruses after intratracheal challenge [7] [8] [9] . SP-A1, -A2 and -D also play a pivotal role in the regulation of inflammatory responses [4, 10, 11] and clearance of apoptotic cells [4, 12, 13] . In mice, SP-A and SP-D have been shown to be nonredundant in the immune defense in vivo [9] .