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Reduced expression of COXs and production of prostaglandin E(2) in patients with nasal polyps with or without aspirin-intolerant asthma

  • 0Immunoallèrgia Respiratòria Clínica i Experimental, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
The Journal of Allergy and Clinical Immunology +

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March 15, 2011

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March 15, 2011

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Summary

This summary is machine-generated.

Altered cyclooxygenase (COX) enzyme activity, specifically reduced prostaglandin E2 (PGE2) production and lack of COX enzyme upregulation, is linked to nasal polyps (NPs) in patients with or without aspirin-intolerant asthma (AIA). This impacts the inflammatory response in nasal tissues.

Area Of Science

  • Biochemistry
  • Immunology
  • Otorhinolaryngology

Background

  • The role of cyclooxygenase (COX) enzymes and their prostaglandin (PG) products in nasal polyp (NP) and aspirin-intolerant asthma (AIA) pathogenesis is debated.
  • Investigating the COX pathway's involvement is crucial for understanding these inflammatory conditions.

Purpose Of The Study

  • To determine the roles of prostaglandin E2 (PGE2), COX-1, COX-2, and PGE2 receptors in the development of NPs and AIA.
  • To measure the expression of these molecules in fibroblasts from nasal mucosa (NM) and NPs.

Main Methods

  • Fibroblasts were isolated from nasal mucosa of control subjects and from nasal polyps of aspirin-tolerant nonasthmatic patients and aspirin-intolerant asthma (AIA) patients.
  • Cultures were stimulated with IL-1β, and PGE2 secretion, COX-1/COX-2 expression, and EP1-EP4 receptor expression were analyzed using ELISA, immunoblotting, and immunofluorescence.

Main Results

  • PGE2 concentrations were significantly lower in IL-1β-stimulated fibroblasts from NP patients, especially those with AIA, compared to controls.
  • IL-1β induced COX-1 and COX-2 expression in control fibroblasts but had minimal effects in fibroblasts from NP patients, particularly those with AIA.
  • IL-1β induced EP2 expression in control fibroblasts but not in fibroblasts from NP patients with or without AIA.

Conclusions

  • Reduced PGE2 production and a lack of COX-1, COX-2, and EP2 upregulation under inflammatory conditions are associated with nasal polyps.
  • These alterations in the COX pathway contribute to the pathogenesis of NPs in patients with or without AIA.

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