Language
English
Publication Date
11-1-2024
Journal
The American Journal of Pathology
DOI
10.1016/j.ajpath.2024.07.011
PMID
39117111
PubMedCentral® Full Text Version
Post-print
Abstract
Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease of preterm infants that is associated with life-long morbidities. Inflammatory insults contribute to BPD pathogenesis. Although the proinflammatory cytokine, IL-17a, plays a role in various neonatal inflammatory disorders, its role in BPD pathogenesis is unclear. To test the hypothesis that blocking IL-17a signaling decreases lipopolysaccharide (LPS)-mediated experimental BPD in neonatal mice, wild-type mice were injected intraperitoneally with phosphate-buffered saline or LPS during the saccular lung developmental phase. Pulmonary IL-17a expression was determined by enzyme-linked immunosorbent assay and by flow cytometry. LPS-injected mice had higher pulmonary IL-17a protein levels and IL-17a
Keywords
Animals, Bronchopulmonary Dysplasia, Interleukin-17, Signal Transduction, Mice, Lipopolysaccharides, Pneumonia, Pulmonary Alveoli, Mice, Inbred C57BL, Disease Models, Animal, Animals, Newborn, Apoptosis, Cell Proliferation
Published Open-Access
yes
Recommended Citation
Goates, Meagan; Shrestha, Amrit; Thapa, Shyam; et al., "Blocking IL-17a Signaling Decreases Lung Inflammation and Improves Alveolarization in Experimental Bronchopulmonary Dysplasia" (2024). Faculty and Staff Publications. 5960.
https://digitalcommons.library.tmc.edu/baylor_docs/5960