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J Pathol. 2018 Jun;245(2):153-159. doi: 10.1002/path.5076. Epub 2018 Apr 18.

Resident alveolar macrophages are master regulators of arrested alveolarization in experimental bronchopulmonary dysplasia.

Author information

1
Department of Lung Development and Remodelling, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
2
Department of Internal Medicine (Pulmonology), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University Giessen, German Center for Lung Research (DZL), Giessen, Germany.
3
Institute of Virology, Philipps University Marburg, Marburg, Germany.
4
Division of General Pediatrics and Neonatology, University Children's Hospital Giessen, Justus Liebig University, Giessen, Germany.

Abstract

Trophic functions for macrophages are emerging as key mediators of developmental processes, including bone, vessel, and mammary gland development. Yolk sac-derived macrophages mature in the distal lung shortly after birth. Myeloid-lineage macrophages are recruited to the lung and are activated under pathological conditions. These pathological conditions include bronchopulmonary dysplasia (BPD), a common complication of preterm birth characterized by stunted lung development, where the formation of alveoli is blocked. No study has addressed causal roles for immune cells in lung alveolarization. We employed antibody-based and transgenic death receptor-based depletion approaches to deplete or prevent lung recruitment of immune cell populations in a hyperoxia-based mouse model of BPD. Neither neutrophils nor exudate macrophages (which might include lung interstitial macrophages) contributed to structural perturbations to the lung that were provoked by hyperoxia; however, cells of the Csf1r-expressing monocyte/macrophage lineage were implicated as causal mediators of stunted lung development. We propose that resident alveolar macrophages differentiate into a population of CD45+ CD11c+ SiglecF+ CD11b+ CD68+ MHCII+ cells, which are activated by hyperoxia, and contribute to disturbances to the structural development of the immature lung. This is the first report that causally implicates immune cells in pathological disturbances to postnatal lung organogenesis. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

KEYWORDS:

alveolarization; bronchopulmonary dysplasia; lung development; macrophage; neonate; neutrophil; organogenesis; trophic

PMID:
29574785
DOI:
10.1002/path.5076

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