Differential regulation of secretion of SP-A and SP-D in neonatal baboons with chronic lung injury (BPO)

Premature baboons delivered at 125 days g.a. (term = 183 days), like premature infants with BPD, have increased vulnerability to infection. Since surfactant proteins A and D are important in host-defense against air-borne microorganisms, part of this susceptibility might be from reduced levels of SP-A and SP-D. Baboons of 125 days gestation age were ventilated with clinically appropriate oxygen for varying times in a clinical setting emphasizing sterile conditions. The animals were divided into two groups. Group 1 animals responded to management with a favorable clinical course and were sacrificed at 6 and 14 days, as scheduled. Group 2 animals were intended for long-term ventilation, but were sacrificed early because of poor clinical prognosis. These animals were ventilated for 5 to 57 days. The results were as follows: Group 1. Tissue SP-A and SP-D generally followed their mRNAs and were equal or greater than adult at 6 and 14 days. Lavage pools, however, were significantly reduced, and the amounts of combined SP-A/SP-D were 18 and 63% of adult. The contribution of SP-D to the combined SP-A/SP-D pool was much greater than in the adult. Group 2 (poor prognosis, early sacrifice). Tissue pools were 40% of adult through 14 days, but equaled adult by 21 days. In contrast, lavage combined SP-A/SP-D never exceeded 7% of adult through 57 days ventilation. SP-D contributed over 30% of this pool, whereas in adult it comprises only 5%. Our findings indicate that chrome lung injury in premature baboons is associated with an apparent defect in he secretion of SP-A but not SP-D. Although SP-D is secreted in amounts greater than in normal adults, the combined SP-A/SP-D pool is still substantially lower, and this may exacerbate the propensity towards infection found in these animals.