2018
DOI: 10.1002/path.5076
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Resident alveolar macrophages are master regulators of arrested alveolarization in experimental bronchopulmonary dysplasia

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 b… Show more

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Cited by 60 publications
(72 citation statements)
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“…Furthermore, the expression of their ligands, Csf1 and Ccl2, was upregulated in the hyperoxia-specific clusters Neutro.2 and Mac.4, respectively(Fig. 6h).These observations are consistent with the study by Kalymbetova et al, where Ccr2 -/and CSF1R-depleted mice developed milder structural changes in hyperoxia-exposed lungs50 .The cell count and transcriptional activity of Mac.3 cells (cluster 4), was stable in normal development, as well as after exposure to hyperoxia (Supplementary Figure 6a-c), and expressed high levels of inflammatory mediators, consistent with data by Gibbings et al51 (Supplementary Figure 6k).The concept of M1/M2 polarization of macrophages has been linked to normal development, as well as to several lung pathologies, including BPD2,52,53 . Consistent with previous studies, our results suggested that the expression of M2 genes was increased in alveolar macrophages during postnatal development 2(Supplementary Figure 6l).Furthermore, hyperoxia enhanced the M1 signature of Mac.2 macrophages and induced a new population of macrophages -Mac.4characterized by the activation of both M1 and M2 genes (Supplementary Figure 6m).…”
supporting
confidence: 91%
“…Furthermore, the expression of their ligands, Csf1 and Ccl2, was upregulated in the hyperoxia-specific clusters Neutro.2 and Mac.4, respectively(Fig. 6h).These observations are consistent with the study by Kalymbetova et al, where Ccr2 -/and CSF1R-depleted mice developed milder structural changes in hyperoxia-exposed lungs50 .The cell count and transcriptional activity of Mac.3 cells (cluster 4), was stable in normal development, as well as after exposure to hyperoxia (Supplementary Figure 6a-c), and expressed high levels of inflammatory mediators, consistent with data by Gibbings et al51 (Supplementary Figure 6k).The concept of M1/M2 polarization of macrophages has been linked to normal development, as well as to several lung pathologies, including BPD2,52,53 . Consistent with previous studies, our results suggested that the expression of M2 genes was increased in alveolar macrophages during postnatal development 2(Supplementary Figure 6l).Furthermore, hyperoxia enhanced the M1 signature of Mac.2 macrophages and induced a new population of macrophages -Mac.4characterized by the activation of both M1 and M2 genes (Supplementary Figure 6m).…”
supporting
confidence: 91%
“…In mice, BPD can be modelled by exposure to hyperoxia, leading to increased inflammation and decreased alveolarisation . These changes are likely mediated through colony‐stimulating factor 1 receptor (Csf1r)‐positive monocytes/macrophages and increases in the pro‐inflammatory cytokine IL‐1β .…”
Section: Inflammatory Responses In Early Life Affect Lung Developmentmentioning
confidence: 99%
“…In the lung, AMs are plastic and may change phenotype depending on the conditions. This can be seen during development and in disease , and may affect macrophage function. Type 2 cytokines such as ILC2‐derived IL‐13 or epithelial‐derived IL‐33 promote AMs to express increased levels of YM1, arginase‐1, CCL17, and mannose receptor .…”
Section: Type 2 Immunity In Murine Lung Development and Regenerationmentioning
confidence: 99%
“…CCR2 mediates recruitment and accumulation of monocytes, dendritic cells and exudative macrophages in response to various infectious stimuli (34)(35)(36). CCR2 signaling is required for lung pro-fibrotic responses in mice (37)(38)(39) and partially mediates hyperoxia-induced hypoalveolarization in immature mice (40). Recent studies implicate a role for repetitive LPS exposure in pulmonary hypoalveolarization and inflammation, including increased CCL2 expression (13,(41)(42)(43).…”
Section: Introductionmentioning
confidence: 99%