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Background <p>To investigate how caffeine inhibited hyperoxia-induced NET formation and protected against bronchopulmonary dysplasia (BPD).</p> Methods <p>The impact of caffeine on NETs secretion in neutrophils triggered by hyperoxia-induced A549 cells was&#xa0;examined. The role of the IL-8/CXCR2 axis in inducing NETs was evaluated using IL-8 and anti-CXCR2 antibody. The impact of caffeine on ERK/p38 MAPK signaling induced by hyperoxia&#xa0;was explored. Finally, a BPD animal model was established to observe the effect of caffeine on hyperoxia-induced lung injury.</p> Results <p>Caffeine reduced hyperoxia’s inhibitory effect on A549 cell activity and apoptosis, and suppressed the increased secretion of NETs by hyperoxia-induced A549 cells. The IL-8/CXCR2 axis was found to enhance NETs secretion to injury A549 cell. Caffeine inhibited IL-8 secretion in hyperoxia-induced A549 cells, suppressing NETs formation. It also inhibited the A2AR-ERK/p38 MAPK pathway to reduce IL-8 secretion. In the BPD animal model, caffeine alleviated hyperoxia-induced lung injury, lowered inflammatory factors and levels of ERK/p38 MAPK phosphorylation, NETs. However, CGS21680 and IL-8 treatment lessened caffeine’s effects.</p> Conclusion <p>Caffeine inhibited A2AR-ERK/p38 MAPK-IL-8 pathway to suppress the formation of NETs for alleviating hyperoxia-induced A549 cell injury. This provides a theoretical basis for developing therapeutic strategies targeting NETs to improve the prognosis of premature infants.</p> Impact <p><UnorderedList Mark="Bullet"> <ItemContent> <p>Caffeine inhibited hyperoxia-induced NETs formation and exerts a protective effect on bronchopulmonary dysplasia (BPD).</p> </ItemContent> <ItemContent> <p>Caffeine reduces hyperoxia-induced A549 cell injury and NETs secretion by inhibiting the A2AR-ERK/p38 MAPK-IL-8 pathway.</p> </ItemContent> <ItemContent> <p>This research offers a new theoretical foundation for comprehending how caffeine improves neonatal BPD.</p> </ItemContent> <ItemContent> <p>These findings provide a theoretical basis for developing therapeutic strategies targeting NETs.</p> </ItemContent> <ItemContent> <p>This research offers new insights for improving the prognosis of premature infants with BPD.</p> </ItemContent> </UnorderedList></p>

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Caffeine inhibited the hyperoxia-induced A2AR-ERK/p38 MAPK-IL-8 pathway in type II alveolar epithelial cells to suppress NETs formation in bronchopulmonary dysplasia

  • 期刊论文

  • 发表日期：

    2026年4月29日

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  • Xijuan Wang,
  • Yanan Song,
  • Lu Yu,
  • Keke Song

摘要

Background

To investigate how caffeine inhibited hyperoxia-induced NET formation and protected against bronchopulmonary dysplasia (BPD).

Methods

The impact of caffeine on NETs secretion in neutrophils triggered by hyperoxia-induced A549 cells was examined. The role of the IL-8/CXCR2 axis in inducing NETs was evaluated using IL-8 and anti-CXCR2 antibody. The impact of caffeine on ERK/p38 MAPK signaling induced by hyperoxia was explored. Finally, a BPD animal model was established to observe the effect of caffeine on hyperoxia-induced lung injury.

Results

Caffeine reduced hyperoxia’s inhibitory effect on A549 cell activity and apoptosis, and suppressed the increased secretion of NETs by hyperoxia-induced A549 cells. The IL-8/CXCR2 axis was found to enhance NETs secretion to injury A549 cell. Caffeine inhibited IL-8 secretion in hyperoxia-induced A549 cells, suppressing NETs formation. It also inhibited the A2AR-ERK/p38 MAPK pathway to reduce IL-8 secretion. In the BPD animal model, caffeine alleviated hyperoxia-induced lung injury, lowered inflammatory factors and levels of ERK/p38 MAPK phosphorylation, NETs. However, CGS21680 and IL-8 treatment lessened caffeine’s effects.

Conclusion

Caffeine inhibited A2AR-ERK/p38 MAPK-IL-8 pathway to suppress the formation of NETs for alleviating hyperoxia-induced A549 cell injury. This provides a theoretical basis for developing therapeutic strategies targeting NETs to improve the prognosis of premature infants.

Impact

Caffeine inhibited hyperoxia-induced NETs formation and exerts a protective effect on bronchopulmonary dysplasia (BPD).

Caffeine reduces hyperoxia-induced A549 cell injury and NETs secretion by inhibiting the A2AR-ERK/p38 MAPK-IL-8 pathway.

This research offers a new theoretical foundation for comprehending how caffeine improves neonatal BPD.

These findings provide a theoretical basis for developing therapeutic strategies targeting NETs.

This research offers new insights for improving the prognosis of premature infants with BPD.