Published ahead of print on May 19, 2004, doi:10.1164/rccm.200402-178OC
Am. J. Respir. Crit. Care Med., Volume 170, Number 5, September 2004, 477-484
A more recent version of this article appeared on September 1, 2004
Submitted on February 10, 2004
Accepted on May 18, 2004
Increased Levels of Hypoxia-sensitive Proteins in Allergic Airway Inflammation
Ignacio Fajardo1, Linda Svensson2, Anders Bucht3, and Gunnar Pejler1*
1 Department of Molecular Biosciences, Swedish University of Agricultural Sciences, The Biomedical Centre, Uppsala, Sweden,
2 Department of Medical Countermeasures, FOI NBC Defence, Umea, Sweden,
3 Department of Medical Countermeasures, FOI NBC Defence, Umea, Sweden; Department of Respiratory Medicine and Allergy, University Hospital, Umea, Sweden
* To whom correspondence should be addressed. E-mail: Gunnar.Pejler{at}vmk.slu.se.
In this study we investigated the alterations in protein levels that are induced by allergic eosinophilic lung inflammation. Lung tissue eosinophilia and sequestration of inflammatory cells in airspaces was provoked by systemic sensitization with ovalbumin followed by repeated inhalation challenge with aerosolized ovalbumin. Proteome alterations in lung tissue and bronchoalveolar lavage fluid, respectively, were examined by 2-dimensional gel electrophoresis followed by identification of proteins by mass spectrometry. Several proteins were markedly increased in inflamed tissue. In particular, several proteins that are known to be associated with hypoxia were elevated, e.g. glycolytic enzymes, glucose-regulated protein 78 kDa, prolyl-4-hydroxylase, peroxiredoxin 1 and arginase. Out of the identified proteins, Ym2 displayed the most clear increase, present at high levels in animals with lung eosinophilia, while being undetectable in controls. Further, the levels of cathepsin S were markedly increased in inflamed tissue. Taken together, this study identifies a number of marker proteins associated with the pathogenesis of allergic lung inflammation and indicates a link between allergic airway inflammation and induction of hypoxia-related gene products
Key words: hypoxia, airway inflammation, asthma, glycolysis, proteomics
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