PMCID: PMC5248953 DOI: 10.1165/rcmb.2016-0006OC
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
American journal of respiratory cell and molecular biology
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
Toll-like receptor signaling; bronchopulmonary dysplasia; neonatal lung injury; nicotinamide adenine dinucleotide phosphate oxidase; sepsis
Menden, Heather; Xia, Sheng; Mabry, Sherry M.; Navarro, Angels; Nyp, Michael F.; and Sampath, Venkatesh, "Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 Regulates LPS-Induced Inflammation and Alveolar Remodeling in the Developing Lung." (2016). Manuscripts, Articles, Book Chapters and Other Papers. 531.