Long‐Living Alveolar Macrophages Modulate Severity of Lung Injury and Postnatal Lung Development in Hyperoxia‐Induced Lung Injury Mouse Model

Despite advances in neonatology, bronchopulmonary dysplasia (BPD) continues to be a serious medical problem with long‐term consequences. Alveolar macrophages are long‐living cells which populate lung soon after birth and maintain their population via proliferation, without contribution from circulating monocytes. Normally alveolar macrophages play an essential role in maintaining lung homeostasis and limiting inflammatory response to the pathogens. We hypothesize that neonatal exposure to hyperoxia, via epigenetic mechanisms, may shape these long‐living alveolar macrophages into pro‐inflammatory cells, which contribute to the development of BPD. We sought to investigate the kinetic and phenotype of alveolar macrophages in a mouse model of BPD and to test whether depletion of hyperoxia‐primed alveolar macrophages and recruitment of the monocyte‐derived alveolar macrophages under the normoxic conditions may improve outcomes in mouse model of hyperoxia‐induced lung injury/BPD.

• Publication year

  2017

• Venue

  The FASEB Journal

• Publication date

  2017-04-01

• Fields of study

  Not labeled

• Identifiers
  DOI 10.1096/fasebj.31.1_supplement.871.3
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

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• No concepts are published for this paper.

• No references are available for this paper.

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