Cyclooxygenase-2 mRNA is downexpressed in nasal polyps from aspirin-sensitive asthmatics

Am J Respir Crit Care Med. 1999 Jul;160(1):291-6. doi: 10.1164/ajrccm.160.1.9808048.


Exogenous prostaglandin E2 (PGE2) given by inhalation almost completely abrogates aspirin-induced asthma and the accompanying increase in cysteinyl-leukotrienes production. Cyclooxygenase (COX) may be present in cells in both constitutive (COX-1) and inducible (COX-2) forms. To increase the production of the potentially protective endogenous PGE2, COX-2 should be upregulated. We hypothesize that an abnormal regulation of COX-2 will predispose patients with asthma to develop aspirin-intolerant asthma/rhinitis (AIAR). We therefore examined the expression of COX-2 messenger RNA (mRNA) in healthy nasal mucosa (n = 11) and in nasal polyps from both patients with AIAR (n = 8) and those with aspirin-tolerant asthma/rhinitis (ATAR) (n = 20). After total mRNA extraction, COX-1 and COX-2 mRNA expression were measured using a reverse transcriptase (RT)-semiquantitative PCR technique. Hybrid primers of COX-1. glyceraldehyde-3-phosphate dehydrogenase (GAPDH) or COX-2. GAPDH were used to create PCR products that were cloned and used as internal standard controls in the competitive PCR reaction. Results are presented as mean +/- standard error of 10(6) molecules of mRNA/micrograms of total RNA. No differences in COX-1 mRNA expression were found between nasal mucosa and nasal polyps from both patients with ATAR and those with AIAR. However, COX-2 mRNA expression in nasal polyps from the AIAR group (0.38 +/- 0.10) was markedly and significantly lower than in polyps from the ATAR group (2.93 +/- 0. 52, sevenfold, p < 0.0001) and nasal mucosa (2.10 +/- 0.54, sixfold, p < 0.01). These findings suggest that an inadequate COX-2 regulation may be involved in AIAR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aspirin / adverse effects*
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • Down-Regulation / genetics
  • Drug Hypersensitivity / genetics*
  • Female
  • Gene Expression Regulation, Enzymologic / physiology
  • Humans
  • Isoenzymes / genetics*
  • Male
  • Membrane Proteins
  • Middle Aged
  • Nasal Mucosa / pathology
  • Nasal Polyps / genetics*
  • Nose Neoplasms / genetics*
  • Prostaglandin-Endoperoxide Synthases / genetics*
  • RNA, Messenger / genetics*


  • Isoenzymes
  • Membrane Proteins
  • RNA, Messenger
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • PTGS1 protein, human
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Aspirin