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
Recommended Citation
Menden HL, Xia S, Mabry SM, Navarro A, Nyp MF, Sampath V. Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 Regulates LPS-Induced Inflammation and Alveolar Remodeling in the Developing Lung. Am J Respir Cell Mol Biol. 2016;55(6):767-778. doi:10.1165/rcmb.2016-0006OC