Effects of IL-1 on the expression of surfactant proteins are dependent on degree of maturity

Glumoff, Virpi; Väyrynen, Outi; Kangas, Tiina; Hallman, Mikko

doi:10.1203/00006450-199809000-00255

Cited by 2 publications

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“…EGF [43] and interferon gamma [44] upregulate SP-A, whereas transforming growth factor beta [45] downregulates SP-A in explants from human fetal lung.…”

Section: Cytokine and Endotoxin Responsiveness Of Sp In Lung Explantsmentioning

confidence: 99%

Cytokines, Pulmonary Surfactant and Consequences of Intrauterine Infection

Hallman

1999

Neonatology

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Excess of inflammatory cytokines is implicated in the sequence of inflammatory diseases during the perinatal period. Specific cytokines induce spontaneous premature labor and accelerate fetal lung maturity in case of chorioamnionitis. In addition, they are involved in the pathogenesis of chronic lung disease, periventricular white matter damage, shock and multiorgan damage. Deficient cytokine response of the immature lung is associated with severe respiratory distress syndrome and persistent fetal circulation syndrome. Surfactant supplementation remains the cornerstone among therapies in the premature infant. Brief courses of glucocorticoids, antioxidants or inhaled nitric oxides remain to be fully evaluated as possible adjunct therapies shortly after birth in small premature infants with severe cardiorespiratory failure.

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“…EGF [43] and interferon gamma [44] upregulate SP-A, whereas transforming growth factor beta [45] downregulates SP-A in explants from human fetal lung.…”

Section: Cytokine and Endotoxin Responsiveness Of Sp In Lung Explantsmentioning

confidence: 99%

Cytokines, Pulmonary Surfactant and Consequences of Intrauterine Infection

Hallman

1999

Neonatology

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Degree of Lung Maturity Determines the Direction of the Interleukin-1– Induced Effect on the Expression of Surfactant Proteins

Glumoff

Väyrynen

Kangas

et al. 2000

Am J Respir Cell Mol Biol

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Intra-amniotic interleukin (IL)-1 increases surfactant components in immature fetal lung, whereas high IL-1 after birth is associated with surfactant dysfunction. Our aim was to investigate whether the fetal age influences the responsiveness of surfactant proteins (SPs) to IL-1. Rabbit lung explants from fetuses at 19, 22, 27, and 30 d of gestation and 1-d-old newborns were cultured in serum-free medium in the presence of recombinant human (rh) IL-1alpha or vehicle. The influence of IL-1alpha on SP-A, -B, and -C messenger RNA (mRNA) content was dependent on the conceptional age. In very immature lung on Day 19, rhIL-1alpha (570 ng/ml for 20 h) increased SP-A, -B, and -C mRNA by 860+/-15%, 314+/-108%, and 64+/-17%, respectively. The increase in SP-A mRNA was evident within 4 to 6 h. IL-1alpha increased the SP-A concentration in alveolar epithelial cells and in the culture medium within 20 h. In contrast, at 27 to 30 d of gestation and in newborns, IL-1alpha decreased SP-C, -B, and -A mRNA by means of 64 to 67%, 48 to 59%, and 12 to 15%, respectively. SP-B protein decreased by 45 to 60%. The decrease in mRNA became evident within 8 to 12 h and was dependent on IL-1 concentration. On Day 27, IL-1alpha accelerated the degradation of SP-B mRNA in the presence of actinomycin D. IL-1 did not increase the degradation rate of SP-A mRNA unless both actinomycin D and cycloheximide were added to the explants. The present findings may explain some of the contrasting associations between inflammatory cytokines and lung diseases during the perinatal period. The determinants of the direction of the IL-1 effect on the expression of SPs remain to be identified.

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Effects of IL-1 on the expression of surfactant proteins are dependent on degree of maturity

Cited by 2 publications

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Cytokines, Pulmonary Surfactant and Consequences of Intrauterine Infection

Cytokines, Pulmonary Surfactant and Consequences of Intrauterine Infection

Degree of Lung Maturity Determines the Direction of the Interleukin-1– Induced Effect on the Expression of Surfactant Proteins

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