Send to:

Choose Destination
See comment in PubMed Commons below

Cyclooxygenase-2 is up-regulated in lung parenchyma of chronic obstructive pulmonary disease and down-regulated in idiopathic pulmonary fibrosis.

Author information

  • 1Servei de Pneumologia i Allèrgia Respiratòria, Institut Clinic de Pneumologia i Cirurgia Toràcica, Barcelona, Spain.



In vitro studies have suggested that fibroblasts from idiopathic pulmonary fibrosis (IPF) may have an impaired induction of cyclooxygenase (Cox)-2. We have investigated Cox-1 and Cox-2 expression in lung tissue from IPF.


Cox-1 and Cox-2 expression were determined using RT-competitive PCR and immunohistochemistry in pulmonary biopsies from IPF (n = 22), chronic obstructive pulmonary disease (COPD) (n = 13), and lung tissue from subjects undergoing pleurodesis for spontaneous pneumothorax (control group, n = 17).


Immunohistochemical analysis showed that the score of Cox-2 positive cells was higher in COPD (1 +/- 0) with respect to fibrosis (0.37 +/- 0.1, p < 0.05) and controls (0.57 +/- 0.2). There were no differences between fibrosis and controls in Cox-2 positive cells. The expression of Cox-2 mRNA was significantly higher in COPD (3.26 +/- 0.72 x 10(6) molecules cDNA/microg total RNA) in comparison to IPF (0.57 +/- 0.17) and controls (0.54 +/- 0.16) (p < 0.001). After IL-1beta stimulation (1-10 ng/ml) Cox-2 mRNA basal expression increased significantly in controls (from 35 +/- 12 to 94 +/- 4 x10(6) molecules cDNA/microg total RNA, p < 0.01) and in COPD (from 38 +/- 8 to 92 +/- 3, p < 0.01). In contrast, no significant changes in Cox-2 mRNA expression were found in IPF (from 30 +/- 12 to 43 +/- 16).


Our results suggest that differences in Cox-2 expression may play a role in the regulation of inflammatory responses in lung diseases. Excessive activity is associated with the development of chronic obstructive lung disease, while a limited activation following pro-inflammatory stimulation might contribute to fibrogenic responses.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Loading ...
    Write to the Help Desk