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Am J Physiol Lung Cell Mol Physiol (November 30, 2001). doi:10.1152/ajplung.00274.2001
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Articles in PresS, published online ahead of print November 30, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00274.2001
Submitted on July 19, 2001
Accepted on November 20, 2001

Regulation of Surfactant Proteins by LPS and Proinflammatory Cytokines in Fetal and Newborn Lung

Outi Vayrynen1*, Virpi Glumoff1, and Mikko Hallman1

1 Department of Pediatrics and Biocenter Oulu, University of Oulu, Oulu, Finland

* To whom correspondence should be addressed. E-mail: ovayryne{at}paju.oulu.fi.

Intra-amniotic LPS and cytokines may decrease respiratory distress syndrome (RDS) and increase chronic lung disease in the newborn. The aim was to identify the primary inflammatory mediators regulating the expression of surfactant proteins (SP) in explants from immature (22-d-old fetus) and mature (30-d term fetus and 2-d newborn) rabbit. In immature lung, IL-1{alpha} and IL-1ß upregulated the expression of SP-A and SP-B. These effects of IL-1 were diminished and SP-C mRNA was additively suppressed in the presence of TNF-{alpha} and either LPS or IFN-{gamma}. LPS, TNF-{alpha} and IFN-{gamma} had no effect alone. In explants from the term fetus and the newborn, LPS, IL-1{alpha} and TNF-{alpha} additively suppressed the SPs. LPS acutely induced IL-1{alpha} in alveolar macrophages in mature lung, but not in the immature lung. IFN-{gamma} that generally has low expression in intrauterine infection, decreased the age-dependence of the other agonists' effects on SPs. Present study serves to explain the variation of the pulmonary outcome following an inflammatory insult. We propose that IL-1 from extrapulmonary source induces the surfactant proteins in premature lung and is responsible for the decreased risk of RDS in intra-amniotic infection.




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