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- W2137375320 abstract "Rationale: Chronic lung disease in the premature infant is characterized by impaired alveolar and vascular development preceded by an increase in lung inflammation and apoptosis. The disease mainly occurs after mechanical ventilation with oxygen rich gas (MV-O2). As the presence of Tumor necrosis factor (TNF)-a has been described in association with disease development, we hypothesized, that its absence will ameliorate changes induced by MV-O2 in a model of the disease in newborn mice. Objective and Methods: 5-6 days old TNF-a knock-out (TNF-a -/- ) and wild type (WT, TNF-a +/+ ) mice received MV with 40%O 2 at 180 breaths/min; controls received 40%O 2 without MV respectively. After 8h, lungs (n=10-12/group) were harvested for histologic, mRNA and protein analysis. Primary myofibroblasts (MFB) from unventilated newborn TNF-a -/- and WT mouse lungs were subjected to mechanical stretch (Flexcell®) and cytokine incubation. Results: Contrary to our expectations, pulmonary chemokine (MCP-1, CXCL-1) and cytokine (IL-1b) expression as well as influx of monocytes was significantly elevated in ventilated TNF-a -/- mice, accompanied by an increase in apoptosis (TUNEL, caspase 3, 8 and 9) when compared to WT mice. These differences potentially resulted from a significant increase in TGF-b signaling in TNF -/- mice after MV-O2 confirmed by an elevated response to TGF-β in MFB from TNF-a -/- mice in vitro in contrast to WT pups. Histological changes were similar in both groups. Conclusion: Decreased TNF-a signaling in newborn mice undergoing MV-O2 results in increased TGF-b activation and apoptosis rather than decreased pulmonary inflammation, which needs to be considered when therapeutic strategies are discussed." @default.
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- W2137375320 date "2013-09-01" @default.
- W2137375320 modified "2023-09-26" @default.
- W2137375320 title "Role of TNF-a in ventilator-induced lung injury in the developing murine lung" @default.
- W2137375320 hasPublicationYear "2013" @default.
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