Surfactant proteins A and D in premature baboons with chronic lung injury (Bronchopulmonary dysplasia). Evidence for an inhibition of secretion.
Surfactant proteins A and D (SP-A and SP-D) are believed to participate in the pulmonary host defense and the response to lung injury. In order to understand the effects of prematurity and lung injury on these proteins, we measured the amounts of SP-A and SP-D and their mRNAs in three groups of animals: (1) nonventilated premature baboon fetuses; (2) neonatal baboons delivered prematurely at 140 d gestation age (ga) and ventilated with PRN O(2); (3) animals of the same age ventilated with 100% O(2) to induce chronic lung injury. In nonventilated fetuses, tissue and lavage SP-A were barely detectable in baboons of 125 and 140 d ga, but they equaled or exceeded adult SP-A concentrations (g/g lung dry wt) at 175 d (term gestation, 185 d). In contrast, SP-D was readily detectable in tissue and lavage at 125 and 140 d ga. When the baboons of 140 d ga were ventilated for 10 d with 100% oxygen to produce chronic lung injury, the tissue concentration of SP-A was five times greater than that of normal adults; SP-D 16-times greater. Despite the sizable tissue pools of SP-A and SP-D, however, lavage SP-A was only 7% of that of normal adults and lavage SP-D just equaled the amount in normal adults. Nevertheless, because SP-D is normally in much lower concentration than is SP-A, their total comprised less than 12% of the SP-A and SP-D found in the lavage of a healthy adult. The results indicate that in chronic lung injury, SP-A is significantly reduced in the alveolar space. SP-D concentration in lavage is about equal to that in normal adults, possibly because of the 16-fold excess in tissue, but the total collectin pool in lavage is still significantly reduced. Because these collectins may bind and opsonize bacteria and viruses, decrements in their amounts may present additional risk to those premature infants who require prolonged periods of ventilatory support.
Awasthi
S
S
Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Coalson
J J
JJ
Crouch
E
E
Yang
F
F
King
R J
RJ
D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D015152:Blotting, Northern; D015153:Blotting, Western; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D001997:Bronchopulmonary Dysplasia / Q000378:metabolism* / Q000473:pathology; D002908:Chronic Disease; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D006023:Glycoproteins / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007231:Infant, Newborn; D010215:Papio; D011510:Proteolipids / Q000378:metabolism*; D037662:Pulmonary Surfactant-Associated Protein A; D037663:Pulmonary Surfactant-Associated Protein D; D037661:Pulmonary Surfactant-Associated Proteins; D011663:Pulmonary Surfactants / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D012121:Respiration, Artificial
D006023:Glycoproteins; D011510:Proteolipids; D037662:Pulmonary Surfactant-Associated Protein A; D037663:Pulmonary Surfactant-Associated Protein D; D037661:Pulmonary Surfactant-Associated Proteins; D011663:Pulmonary Surfactants; D012333:RNA, Messenger