ArticlePediatric research2026
Proinflammatory monocyte-derived granulocyte-macrophage colony-stimulating factor fuels airway inflammation in bronchopulmonary dysplasia.
Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Authors and funding
10 authors.
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Abstract
backgroundBronchopulmonary dysplasia (BPD) remains a leading cause of morbidity and long-term respiratory complications in preterm neonates. Effective strategies for moderate-severe BPD are currently lacking.
methodsTracheal aspirate (TA) samples were collected from 62 preterm neonates, and the immune cell composition was analyzed using multicolor flow cytometry. Subsequently, CD14
resultsCD14
conclusionsGM-CSF derived from airway pro-inflammatory monocytes exacerbated inflammation in preterm neonates with BPD, particularly in moderate-severe cases. Baricitinib emerges as a promising therapeutic option, offering new hope for mitigating the inflammatory burden associated with moderate-severe BPD. IMPACT: Moderate-to-severe bronchopulmonary dysplasia in preterm infants is closely linked to the sustained production of high levels of GM-CSF (granulocyte-macrophage colony-stimulating factor) by airway inflammatory monocytes. We propose a local GM-CSF-driven inflammatory positive-feedback loop in airway of patients with BPD. Interrupting the downstream GM-CSF signaling pathway may hold promise as the next effective therapeutic strategy.
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Registered trials
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