CD11b(+) Mononuclear Cells Mitigate Hyperoxia-induced Lung Injury in Neonatal Mice.

Publication Type:

Journal Article


American journal of respiratory cell and molecular biology (2015)


Bronchopulmonary dysplasia (BPD) is a common consequence of life-saving interventions for infants born with immature lungs. Resident tissue myeloid cells regulate lung pathology, but their role in BPD is poorly understood. To determine the role of lung interstitial myeloid cells in neonatal responses to lung injury, we exposed newborn mice to hyperoxia, a neonatal mouse lung injury model with features of human BPD. In newborn mice raised in normoxia, we identified a CD45+F4/80+CD11b+CD71+ population of cells in lungs of neonatal mice present in significantly greater percentages than in adult mice. In response to hyperoxia, surface marker and gene expression in whole lung macrophages/monocytes was biased to an alternatively activated phenotype. Partial depletion of these CD11b+ mononuclear cells using CD11b-diptheria toxin receptor (DTR) transgenic mice resulted in 60% mortality by 40 h of hyperoxia exposure with more severe lung injury, perivascular edema, alveolar hemorrhage, compared to DT-treated CD11b-DTR negative controls, which displayed no mortality. These results identify and anti-inflammatory population of CD11b+ mononuclear cells that are protective in hyperoxia-induced neonatal lung injury in mice and suggest that enhancing their beneficial functions may be a treatment strategy in infants at risk for BPD.