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Published ahead of print on June 7, 2004, doi:10.1164/rccm.200311-1607OC

Am. J. Respir. Crit. Care Med., Volume 170, Number 6, September 2004, 633-640

A more recent version of this article appeared on September 15, 2004
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Submitted on November 25, 2003
Accepted on June 4, 2004

Heme Oxygenase-1 in Cystic Fibrosis and Cytoprotective Effects Against Pseudomonas aeruginosa

Hailan Zhou1, Fuhua Lu1, Christopher Latham1, Dani S Zander2, and Gary A Visner1*

1 Department of Pediatrics, University of Florida, Gainesville, FL, USA, 2 Department of Pathology, University of Texas Medical School at Houston, Houston, TX, USA

* To whom correspondence should be addressed. E-mail: visnega{at}peds.ufl.edu.

Inflammation and oxidative stress play important roles in cystic fibrosis (CF) lung disease. Inflammatory/oxidant mediated induction of heme oxygenase 1 (HO-1) is believed to be a cytoprotective response. This study examined HO-1 expression in lung samples from patients with CF using immunohistochemistry and quantitative RT-PCR. In addition, we evaluated myeloperoxidase staining as a marker of acute inflammation and potentially an increase in oxidant stress, and Prussian blue and ferritin staining to assess iron status of the lung. Macrophage HO-1 staining was increased in diseased lungs as compared to normal controls, and correlated with myeloperoxidase staining. Quantitative RT-PCR further supported an increase in HO-1 expression in CF lung disease. Although iron staining was minimal, ferritin staining was increased in diseased lungs in concert with HO-1 staining. To determine if HO-1 induction was cytoprotective, we evaluated a CF airway epithelial cell line, IB3.1, in response to Pseudomonas aeruginosa- induced injury/apoptosis in cells overexpressing HO-1 by either transient or stable transfection of pcDNA3.1/HO-1 construct. Overexpression of HO-1 resulted in protection against Pseudomonas aeruginosa induced injury/apoptosis. This suggests that the induction of HO-1 in patients with CF is a cytoprotective event, and that augmenting its expression is a potential therapy against bacterial injury.
Key words: heme oxygenase-1, cystic fibrosis, oxidative stress, Pseudomonas aeruginosa, Cyclooxygenase-2




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