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1 Children's Hospital Medical Center, Division of Pulmonary Biology, Cincinnati, Ohio 45229-3039; and 2 TVW Telethon Institute for Child Health Research, Division of Clinical Science, University of Western Australia, Perth, Australia 6001
Although
the surface properties of surfactant protein (SP)-B and SP-C are
similar, the contributions that either protein may make to lung
function have not been identified in vivo. Mutations in SP-B cause
lethal respiratory failure at birth; however, SP-B null mice are
deficient in both SP-B and SP-C. To identify potential contributions of
SP-C to lung function in vivo, the following transgenic mice were
generated and exposed to 95% O2 for 3 days: (SP-B+/+,SP-C+/+),
(SP-B+/+, SP-C
/),
(SP-B+/,SP-C+/+),
(SP-B+/,SP-C+/),
and (SP-B+/,SP-C/).
Hyperoxia altered pressure-volume curves in mice that were heterozygous
for SP-B, and these values were further decreased in
(SP-B+/,SP-C/) mice. Likewise, alveolar
interleukin (IL)-6 and IL-1
were maximally increased by
O2 exposure of (SP-B+/,SP-C/)
mice compared with the other genotypes. Lung hysteresivity was lower in
the (SP-B+/,SP-C/) mice. Surfactant
isolated from (SP-B+/+,SP-C/) and
(SP-B+/,SP-C/) mice failed to stabilize
the surface tension of microbubbles, showing that SP-C plays a role in
stabilization or recruitment of phospholipid films at low bubble
radius. Genetically decreased levels of SP-B combined with superimposed
O2-induced injury reveals the distinct contribution of SP-C
to pulmonary function in vivo.
lung injury; transgenic mice; saturated phosphatidylcholine; surfactant protein-B and -C
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