Hemorrhagic shock induces G-CSF expression in bronchial epithelium

Christian Hierholzer, Edward Kelly, Katsuhiko Tsukada, Eric Loeffert, Simon Watkins, Timothy R. Billiar, David J. Tweardy*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


Hemorrhagic shock (HS) initiates a series of inflammatory processes that includes the activation of polymorphonuclear granulocytic neutrophils (PMN). We tested the hypothesis that HS induces granulocyte colony-stimulating factor (G-CSF), a cytokine that augments PMN effector functions, in the lungs of rats. Sprague-Dawley rats were subjected to compensated or decompensated HS followed by resuscitation and death at 4 or 8 h. Animals subjected to HS demonstrated acute lung injury with PMN infiltration, edema, and hypoxia. Using semiquantitative reverse transcriptase-polymerase chain reaction, we detected a 1.9- to 7.1-fold increase in G-CSF mRNA levels in the lung of animals subjected to HS compared with sham controls. Levels of G-CSF mRNA increased with increased duration of the ischemic phase of resuscitated shock. In situ hybridization revealed that bronchoepithelial cells were the major cellular site of G-CSF mRNA. Thus production of G-CSF mRNA by bronchoepithelial cells is dramatically increased in a rat model of HS that also demonstrated lung injury. Increased local G-CSF levels may contribute to PMN recruitment and activation and resultant lung injury in HS.

Original languageEnglish
Pages (from-to)L1058-L1064
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number5 17-5
StatePublished - 1997
Externally publishedYes


  • Bronchoepithelial cell
  • Granulocyte colony-stimulating factor
  • Inflammation
  • Lung


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