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G‐CSF instillation into rat lungs mediates neutrophil recruitment, pulmonary edema, and hypoxia
Author(s) -
Hierholzer Christian,
Kelly Edward,
Lyons Valerie,
Roedling Eva,
Davies Paul,
Billiar Timothy R.,
Tweardy David J.
Publication year - 1998
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.63.2.169
Subject(s) - hypoxia (environmental) , biology , pulmonary edema , edema , lung , immunology , pharmacology , medicine , oxygen , chemistry , organic chemistry
Activated neutrophils (PMN) have been implicated in the pathogenesis of adult respiratory distress syndrome (ARDS). Granulocyte colony‐stimulating factor (G‐CSF) is essential for PMN production and activation of PMN functions. We have recently shown that levels of G‐CSF mRNA in a rat model of hemorrhagic shock correlated with severity of shock, PMN infiltration, pulmonary edema, and hypoxia. To determine whether increased tissue levels of G‐CSF contribute to PMN recruitment and PMN‐mediated injury, we instilled G‐CSF into the lungs by intratracheal injection. Animals treated with G‐CSF became hypoxic, hypocapnic, and alkalotic and demonstrated increased BAL fluid cellularity compared with control animals. The wet‐to‐dry ratio increased significantly after G‐CSF instillation and peaked at 12 h. Histological examination of the lungs from G‐CSF‐treated rats revealed marked edema and increased PMN within the interstitium and alveoli. These results indicate that the presence of G‐CSF alone in the lung can lead to recruitment of PMN, lung injury, and impaired pulmonary function, suggesting that local production of G‐CSF may contribute to the development of lung damage and possibly ARDS in the setting of resuscitated hemorrhagic shock. J. Leukoc. Biol . 63: 169–174; 1998.