SP-A DEFICIENCY IN PRIMATE MODEL OF BRONCHOPULMONARY DYSPLASIA WITH INFECTION - IN-SITU MESSENGER-RNA AND IMMUNOSTAINS

The surfactant protein secretory cells in airway and alveolar epitheli um were studied in premature baboons with bronchopulmonary dysplasia a nd superimposed infection. PRN animals were delivered by hysterotomy a t 140 d gestational age and ventilated on clinically appropriate oxyge n for a 16-d experimental period. To assess 0 time and sacrifice time gestational parameters, 140 and 156 d were studied. BPD animals were d elivered at 140 d and ventilated with positive-pressure ventilation an d an FIO2 of 1.0 for 11 d followed by 5 d of oxygen sufficient to main tain PA(O2) at 40 to 50 mm Hg. BPD-infected animals were comparably ve ntilated and treated like the BPD group except that 10(B) E. coli orga nisms were endotracheally instilled on Day 11. In situ hybridization s tudies for mRNA expression of SP-A, SP-B, and SP-C revealed that an SP -A mRNA deficiency, present at 140 d, persisted in the BPD and BPD-inf ected groups, whereas SP-A mRNA was abundant in PRN and 156 d gestatio n control groups. SP-B and SP-C mRNA expression in the two hyperoxical ly injured groups was particularly extensive in cells around peribronc hiolar and perivascular sites. Immunostaining with SP-A, SP-B, and SP- C antibodies showed variable staining patterns. The study clearly demo nstrates that a deficiency of SP-A mRNA expression persists in chronic lung injury and that variable protein staining patterns are manifeste d depending upon the underlying pathology.