Document Type

Article

Publication Date

12-1-2016

Identifier

PMCID: PMC5248953 DOI: 10.1165/rcmb.2016-0006OC

Abstract

In premature infants, sepsis is associated with alveolar simplification manifesting as bronchopulmonary dysplasia. The redox-dependent mechanisms underlying sepsis-induced inflammation and alveolar remodeling in the immature lung remain unclear. We developed a neonatal mouse model of sepsis-induced lung injury to investigate whether nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) regulates Toll-like receptor (TLR)-mediated inflammation and alveolar remodeling. Six-day-old NOX2

Journal Title

American journal of respiratory cell and molecular biology

Volume

55

Issue

6

First Page

767

Last Page

778

MeSH Keywords

Acute Disease; Animals; Biomarkers; Cytokines; Extracellular Matrix; Lipopolysaccharides; Membrane Glycoproteins; Mice; NADPH Oxidase 2; NADPH Oxidases; NF-kappa B; Pneumonia; Pulmonary Alveoli; Sepsis; Toll-Like Receptors; Transcription Factor AP-1

Keywords

Toll-like receptor signaling; bronchopulmonary dysplasia; neonatal lung injury; nicotinamide adenine dinucleotide phosphate oxidase; sepsis

Collection

Neonatology

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