期刊
PEDIATRIC RESEARCH
卷 56, 期 6, 页码 907-913出版社
NATURE PUBLISHING GROUP
DOI: 10.1203/01.PDR.0000145274.47221.10
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- NHLBI NIH HHS [HL56399] Funding Source: Medline
Tracheal aspirate IL-8 concentration and airway epithelial cell IL-8 expression are each increased in premature infants undergoing mechanical ventilation. We sought to determine the cytokines responsible for IL-8 expression in this context. Tracheal aspirates were collected from 18 mechanically ventilated premature infants. IL-8 protein abundance was high in tracheal aspirates from ventilated premature infants (mean, 5806 4923 pg/mL). IL-1alpha (mean, 20 +/- 6 pg/mL), IL-1beta (mean 67 +/- 46 pg/mL), and tumor necrosis factor (TNF)-alpha (mean, 8 +/- 2 pg/mL) were also found. Incubation of tracheal aspirates with 16HBE14o- human bronchial epithelial cells increased IL-8 protein in both cell lysates and supernatants, as well as transcription from the IL-8 promoter. Aspirates also induced nuclear factor (NF)-kappaB activation. Mutation of the IL-8 promoter NF-kappaB site abolished aspirate-induced IL-8 transcription. Endotoxin concentrations in the tracheal aspirates were negligible and incapable of inducing IL-8 promoter activity. Finally, incubation of tracheal aspirates with a neutralizing antibody against IL-1beta reduced epithelial cell IL-8 production, whereas neutralizing antibodies against IL-1alpha and TNF-alpha had no effect. We conclude that airway fluid from mechanically ventilated premature infants contains soluble factors capable of inducing airway epithelial cell IL-8 expression via a NF-kappaB-dependent pathway, and that IL-1beta plays a specific role in this process.
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