Anti-neutrophil chemokine preserves alveolar development in hyperoxia-exposed newborn rats.

@article{Auten2001AntineutrophilCP,
  title={Anti-neutrophil chemokine preserves alveolar development in hyperoxia-exposed newborn rats.},
  author={Richard L Auten and S. Nicholas Mason and David Tanaka and Karen E. Welty-Wolf and Mary H Whorton},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2001},
  volume={281 2},
  pages={L336-44}
}
Inflammation may contribute to lung injury and impaired alveolar development in bronchopulmonary dysplasia. We treated hyperoxia-exposed newborn rats with antibodies to the neutrophil chemokine cytokine-induced neutrophil chemoattractant-1 (CINC-1) during 95% O2 exposure to reduce adverse effects of hyperoxia-induced inflammation on lung development. Rats were exposed at birth to air, 95% O2, or 95% O2 + anti-CINC-1 (injected on days 3 and 4). Bromodeoxyuridine (BrdU) was injected 6 h before… CONTINUE READING

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Mentioned Connections BETA
Inflammation may contribute to lung injury and impaired alveolar development in bronchopulmonary dysplasia .
Blockade of neutrophil influx in newborns may avert early lung injury and avoid alveolar developmental arrest that contributes to bronchopulmonary dysplasia .
Inflammation may contribute to lung injury and impaired alveolar development in bronchopulmonary dysplasia .
Inflammation may contribute to lung injury and impaired alveolar development in bronchopulmonary dysplasia .
Inflammation may contribute to lung injury and impaired alveolar development in bronchopulmonary dysplasia .
Blockade of neutrophil influx in newborns may avert early lung injury and avoid alveolar developmental arrest that contributes to bronchopulmonary dysplasia .
Inflammation may contribute to lung injury and impaired alveolar development in bronchopulmonary dysplasia .
OxygenNo subtypeHyperoxia
We treated hyperoxia - exposed newborn rats with antibodies to the neutrophil chemokine cytokine - induced neutrophil chemoattractant-1 ( CINC-1 ) during 95% O2 exposure to reduce adverse effects of hyperoxia - induced inflammation on lung development .
We treated hyperoxia - exposed newborn rats with antibodies to the neutrophil chemokine cytokine - induced neutrophil chemoattractant-1 ( CINC-1 ) during 95% O2 exposure to reduce adverse effects of hyperoxia - induced inflammation on lung development .
Inflammation may contribute to lung injury and impaired alveolar development in bronchopulmonary dysplasia .
HyperoxiaNo subtypeOxygen
We treated hyperoxia - exposed newborn rats with antibodies to the neutrophil chemokine cytokine - induced neutrophil chemoattractant-1 ( CINC-1 ) during 95% O2 exposure to reduce adverse effects of hyperoxia - induced inflammation on lung development .
We treated hyperoxia - exposed newborn rats with antibodies to the neutrophil chemokine cytokine - induced neutrophil chemoattractant-1 ( CINC-1 ) during 95% O2 exposure to reduce adverse effects of hyperoxia - induced inflammation on lung development .
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