Research collaborations with the University of Southampton

Abnormalities of surfactant in a heterogenous population of children admitted to PICU and ventilated for Acute Hypoxaemic Respiratory Failure

Michael Marsh (Ex-Director PICU, present Medical Director, SUHT; Professor Tony Postle (Professor of Developmental Biochemistry, Division of Infection, Inflammation and Immunity, University of Southampton and David Todd (PICU, SUHT and the Department of Physiology, Flinders University, Adelaide, Australia).

This collaboration was lead by Michael Marsh and Professor Postle


To explore the pathophysiology of acute lung injury in children.


Prospective cohort study.


Regional University Hospital, pediatric intensive care unit.


Children without pre-existing lung disease who developed acute lung injury (ALI) and were subsequently intubated, were eligible for inclusion in the study. Children without lung injury and who were intubated for minor surgical procedures acted as controls.


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

Measurements and main results

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


Changes to the PC profile, surfactant proteins, and inflammatory markers in BALF and plasma in children with acute lung injury are consistent with an increase in alveolar/blood permeability and an increase in the alveolar concentration of inflammatory cell membrane degradation products. These changes are due to alveolar capillary membrane damage and cellular infiltration.