As one major function SP-A displays a protective role of the molecule in pulmonary host defense by interacting with various infectious agents such as bacteria, fungi and viruses. SP-A deficient knock-out mice -compared to wild type animals -are susceptible to infections with Pseudomonas aeruginosa [13] and the clearance of group B streptococcus is slower [14] . In accordance the defense of SP-A deficient mice against Respiratory Syncytial Virus (RSV) has been shown to be reduced and may be restored by exogenous SP-A administration [15] [16] [17] .