Surfactant phospholipids, surfactant proteins, and inflammatory markers during acute lung injury in children.
OBJECTIVE
To explore the pathophysiology of acute lung injury in children.


METHODS
Prospective cohort study.


METHODS
Regional University Hospital, pediatric intensive care unit.


METHODS
Children without a preexisting lung injury who developed acute lung injury and were intubated were eligible for the study. Children without lung injury and intubated for minor surgical procedures acted as controls.


METHODS
Bronchoalveolar lavage fluid and blood were collected on days 1 to 4, weekly, and immediately before extubation during acute lung injury. Molecular species compositions of phosphatidylcholine were determined by electrospray ionization mass spectrometry of lipid extracts of bronchoalveolar lavage fluid supernatants. Surfactant proteins A, B, and D and interleukin-8 were measured in bronchoalveolar lavage fluid and plasma by enzyme-linked immunosorbent assay and Western blotting.


RESULTS
Eighteen children with acute lung injury were enrolled in the study and compared with eight controls. In children with acute lung injury, there were significant changes in the bronchoalveolar lavage fluid phosphatidylcholine species. Bronchoalveolar lavage fluid dipalmitoyl phosphatidylcholine (PC 16:0/16:0) and palmitoyl-myristoyl phosphatidylcholine (PC 16:0/14:0) significantly deceased during acute lung injury (p < .001 and p < .001, respectively), whereas oleoyl-linoleoyl PC (18:1/18:2), palmitoyl-linoleoyl PC (16:0/18:2) and stearoyl-linoleoyl PC (18:0/18:2) characteristic of plasma PC were significantly increased (p < .05, p < .02, and p < .05 respectively), as well as palmitoyl-oleoyl PC (16:0/18:1), and stearoyl-arachidonoyl PC (18:0/20:4) which are characteristic of cell membranes (p < .02, and p < .02, respectively). There were no significant changes to bronchoalveolar lavage fluid, surfactant protein A or B levels compared with controls during acute lung injury, whereas bronchoalveolar lavage fluid, surfactant protein D, and interleukin-8 levels significantly increased (p < .05 and p < .02, respectively). In plasma during acute lung injury, there were significant increases in surfactant proteins A, B, and D, and interleukin-8 (p < .001, p < .001, p < .05, and p < .001, respectively).


CONCLUSIONS
Changes to the phosphatidylcholine profile, surfactant proteins, and inflammatory markers of bronchoalveolar lavage fluid and plasma in children with acute lung injury are consistent with an alveolar/blood leakage and inflammatory cell membrane degradation products. These changes are due to alveolar capillary membrane damage and cellular infiltration.
Todd
David A
DA
Centre for Newborn Care, Canberra Hospital, Garran, Woden ACT, Australia. David.Todd@act.gov.au
Marsh
Michael J
MJ
George
Anne
A
Henderson
Neil G
NG
Barr
Heather
H
Sebastian
Seby
S
Clark
Graeme T
GT
Koster
Grielof
G
Clark
Howard W
HW
Postle
Anthony D
AD
D055371:Acute Lung Injury / Q000503:physiopathology*; D015415:Biomarkers / Q000378:metabolism; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007249:Inflammation / Q000175:diagnosis* / Q000503:physiopathology; D015278:Intensive Care Units, Pediatric; D016209:Interleukin-8 / Q000378:metabolism; D007442:Intubation, Intratracheal; D008074:Lipoproteins / Q000378:metabolism; D008297:Male; D010743:Phospholipids / Q000032:analysis*; D011446:Prospective Studies; D011663:Pulmonary Surfactants / Q000032:analysis*; D012128:Respiratory Distress Syndrome / Q000503:physiopathology
D015415:Biomarkers; D016209:Interleukin-8; D008074:Lipoproteins; D010743:Phospholipids; D011663:Pulmonary Surfactants