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1 Divisions of Neonatology and Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA; Neonatology, St. Vincent Children's Hospital, Indianapolis, IN, USA
2 Divisions of Neonatology and Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA; Department of Neonatology, Children's Mercy Hospital, Kansas City, MO, USA
3 Divisions of Neonatology and Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA
* To whom correspondence should be addressed. E-mail: tim.weaver{at}cchmc.org.
Surfactant protein B (SP-B) is required for function of newborn and adult lung, and partial deficiency has been associated with susceptibility to lung injury. In the present study, transgenic mice were produced in which expression of SP-B in type II epithelial cells was conditionally regulated. Concentrations of SP-B were maintained at 60-70% of that normally present in control. Immunostaining for SP-B demonstrated cellular heterogeneity in expression of the protein. In subsets of type II cells in which SP-B staining was decreased, immunostaining for proSP-C was increased and lamellar body ultrastructure was disrupted consistent with focal SP-B deficiency. FACS analyses of freshly isolated type II cells identified a population of cells with low SP-B content and a smaller population with increased SP-B content, confirming nonuniform expression of the SP-B transgene. Focal airspace enlargement, without cellular infiltration or inflammation was observed. Pressure-volume curves indicated that maximal tidal volume was unchanged; however, hysteresis was modestly altered and residual volumes were significantly decreased in the SP-B deficient mice. Chronic, non-uniform SP-B deficiency perturbed pulmonary function and caused airspace enlargement.
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