SP-A deficiency in primate model of bronchopulmonary dysplasia with infection: In situ mRNA and immunostains

J. J. Coalson, R. J. King, F. Yang, V. Winter, J. A. Whitsett, R. A. Delemos, S. R. Seidner

Research output: Contribution to journalArticle

53 Scopus citations

Abstract

The surfactant protein secretory cells in airway and alveolar epithelium were studied in premature baboons with bronchopulmonary dysplasia and superimposed infection. PRN animals were delivered by hysterotomy at 140 d gestational age and ventilated on clinically appropriate oxygen for a 16-d experimental period. To assess 0 time and sacrifice time gestational parameters, 140 and 156 d were studied. BPD animals were delivered at 140 d and ventilated with positive-pressure ventilation and an FIO2 of 1.0 for 11 d followed by 5 d of oxygen sufficient to maintain PAO2 at 40 to 50 mm Hg. BPD-infected animals were comparably ventilated and treated like the BPD group except that 108 E. coli organisms were endotracheally instilled on Day 11. In situ hybridization studies 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-infected groups, whereas SP-A mRNA was abundant in PRN and 156 d gestation control groups. SP-B and SP-C mRNA expression in the two hyperoxically injured groups was particularly extensive in cells around peribronchiolar and perivascular sites. Immunostaining with SP-A, SP-B, and SP-C antibodies showed variable staining patterns. The study clearly demonstrates that a deficiency of SP-A mRNA expression persists in chronic lung injury and that variable protein staining patterns are manifested depending upon the underlying pathology.

Original languageEnglish (US)
Pages (from-to)854-866
Number of pages13
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume151
Issue number3 I
StatePublished - Jan 1 1995

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

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