Research

Migrating leukocytes are the source of Peroxiredoxin V during inflammation in the airways

Raisa I Krutilina³ , Andrei V Kropotov^1,3 , Christian Leutenegger^2,3 and Vladimir B Serikov³

¹  Institute of Cytology Russian Academy of Sciences, St. Petersburg, 194021, Russia

²  University of California, Davis, Davis, CA 95616, USA

³  Children's Hospital Oakland Research Institute, Oakland, CA 94609, USA

author email corresponding author email

Journal of Inflammation 2006, 3:13doi:10.1186/1476-9255-3-13

Published:	4 October 2006

Abstract

Background

We characterized changes in expression of the antioxidant protein Peroxiredoxin V (PRXV) during airway inflammation.

Methods

Studies in anesthetized rats and mice; PRXV expression determined by Western blot analyses and immunohistochemistry; PRXV m-RNA expression determined by Taq-Man RT-PCR.

Results

Bacterial lung inflammation did not change expression of PRXV in murine epithelia but produced massive influx of leukocytes highly expressing PRXV. Endotoxin and f-MLP induced leukocyte migration in rat trachea but did not change mRNA levels and PRXV protein expression in tracheal epithelial cells. In primary airway cell culture (cow), alveolar epithelial cells A549, or co-culture of A549 with murine macrophages RAW264.7, exposure to live bacteria increased expression of PRXV, which required serum. PRXV was secreted in vitro by epithelial and immune cells.

Conclusion

Inflammation increased expression of PRXV in airways by at least 2 mechanisms: cell population shift by massive influx of leukocytes expressing PRXV, and moderate post-transcriptional up-regulation of PRXV in epithelial cells.