Boggaram V

Dinarello CA.

Haddad JJ

Hoshino K

Kuroki Y

Le J

Mikko Hallman

Outi Väyrynen

Prescott SL

Romero R

Sone S

Stadler J

Ulich TR

Virpi Glumoff

Watterberg KL

Intra-amniotic lipopolysaccharide (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-day-old fetus) and mature (30-day term fetus and 2-day-old newborn) rabbits. In immature lung, interleukin (IL)-1α and IL-1β upregulated the expression of SP-A and SP-B. These effects of IL-1 were diminished, and SP-C mRNA was suppressed additively in the presence of tumor necrosis factor (TNF)-α and either LPS or interferon (IFN)-γ. LPS, TNF-α, or IFN-γ had no effect alone. In explants from the term fetus and the newborn, LPS, IL-1α, and TNF-α additively suppressed the SPs. LPS acutely induced IL-1α in alveolar macrophages in mature lung but not in the immature lung. IFN-γ that generally has low expression in intrauterine infection decreased the age dependence of the other agonists' effects on SPs. The present study serves to explain the variation of the pulmonary outcome after an inflammatory insult. We propose that IL-1 from extrapulmonary sources induces the SPs in premature lung and is responsible for the decreased risk of RDS in intra-amniotic infection.</jats:p

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AJP Lung Cellular and Molecular Physiology

Regulation of surfactant proteins by LPS and proinflammatory cytokines in fetal and newborn lung

Regulation of surfactant proteins by LPS and proinflammatory cytokines in fetal and newborn lung

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