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Published on: October 19, 2013
Prevention of hyperoxia-mediated pulmonary inflammation in neonatal rats by caffeine
Ulrike Weichelt1, Ruhuye Cay, Thomas Schmitz
1Charité University Medical Centre, Berlin, Germany.
Insights
Caffeine protects preterm infants from lung injury caused by high oxygen levels. This study shows caffeine reduces inflammation and immune cell infiltration in neonatal rat lungs exposed to hyperoxia.
Area of Science:
- Neonatal physiology
- Pulmonary medicine
- Pharmacology
Background:
- Elevated oxygen concentrations in preterm infants are linked to increased chemokine levels and bronchopulmonary dysplasia (BPD).
- Caffeine administration is known to reduce BPD rates in preterm infants.
Purpose of the Study:
- To investigate if caffeine protects infant rats from hyperoxia-induced lung injury.
- To determine if caffeine reduces pulmonary chemokine expression and leukocyte influx following hyperoxia.
Main Methods:
- Infant rats were exposed to 80% oxygen for 24 hours, with or without caffeine administration (10 mg/kg).
- Pulmonary expression of CXC chemokines (cytokine-induced neutrophil chemoattractant-1, macrophage inflammatory protein-2), CC-chemokine (monocyte chemoattractant protein-1), and pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-6) was measured by real-time PCR.
- Leukocyte influx (CD11b+, ED-1+, myeloperoxidase+) was assessed.
Main Results:
- Hyperoxia exposure led to pulmonary recruitment of neutrophils and macrophages.
- High oxygen upregulated pulmonary chemokines and pro-inflammatory cytokines.
- Caffeine administration attenuated chemokine and cytokine upregulation and reduced leukocyte influx.
Conclusions:
- Caffeine confers protection against hyperoxia-induced lung injury in neonatal rats.
- Caffeine's protective effects in the neonatal lung are partly mediated by reducing pulmonary inflammation.
Abstract:
In preterm human infants, briefly elevated concentrations of oxygen are associated with a prolonged increase in blood chemokine concentrations and the development of bronchopulmonary dysplasia (BPD). Caffeine given to preterm infants for the prevention or treatment of apnoea has been shown to reduce the rate of BPD. We tested the hypotheses that infant rats exposed to a combination of caffeine and hyperoxia would be less susceptible to lung injury than those exposed to hyperoxia alone and that caffeine decreases the pulmonary tissue expression of chemokines and leukocyte influx following hyperoxia. Using 6-day-old rat pups, we demonstrated that 24 h of 80% oxygen exposure caused pulmonary recruitment of neutrophils and macrophages. High levels of oxygen upregulated the expression of: the CXC chemokines, cytokine-induced neutrophil chemoattractant-1 and macrophage inflammatory protein-2; the CC-chemokine monocyte chemoattractant protein-1; the pro-inflammatory cytokines tumour necrosis factor-α and interleukin-6, as measured by realtime PCR after the administration of caffeine (10 mg · kg(-1) body weight); and attenuated chemokine and cytokine upregulation, as well as the influx of CD11b(+), ED-1(+) and myeloperoxidase(+) leukocytes. These experiments suggest that protective effects of caffeine in the neonatal lung are mediated, at least in part, by reduction of pulmonary inflammation.