Anti-CCL2 therapy reduces oxygen toxicity to the immature lung

Oxygen toxicity constitutes a key contributor to bronchopulmonary dysplasia (BPD). Critical step in the pathogenesis of BPD is the inflammatory response in the immature lung with the release of pro-inflammatory cytokines and the influx of innate immune cells. Identification of efficient therapies to...

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Bibliographic Details
Published in:Cell death discovery 2024-07, Vol.10 (1), p.311-12, Article 311
Main Authors: Shahzad, Tayyab, Dong, Ying, Behnke, Nina K., Brandner, Julia, Hilgendorff, Anne, Chao, Cho-Ming, Behnke, Judith, Bellusci, Saverio, Ehrhardt, Harald
Format: Article
Language:English
Subjects:
692/308/3187
692/420/256/2515
692/699/1785
Apoptosis
Biochemistry
Biomedical and Life Sciences
Blocking antibodies
CD14 antigen
CD16 antigen
Cell Biology
Cell Cycle Analysis
Cell death
Endothelial cells
Hyperoxia
Inflammation
Leukocytes (neutrophilic)
Life Sciences
Lungs
Macrophages
Mechanical ventilation
Mesenchymal stem cells
Monocyte chemoattractant protein 1
Morphometry
Pathogenesis
Stem Cells
Toxicity
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Summary:Oxygen toxicity constitutes a key contributor to bronchopulmonary dysplasia (BPD). Critical step in the pathogenesis of BPD is the inflammatory response in the immature lung with the release of pro-inflammatory cytokines and the influx of innate immune cells. Identification of efficient therapies to alleviate the inflammatory response remains an unmet research priority. First, we studied macrophage and neutrophil profiles in tracheal aspirates of n  = 103 preterm infants
ISSN:2058-7716
2058-7716
DOI:10.1038/s41420-024-02073-5