Inflammatory genes in nasal polyposis

Curr Opin Otolaryngol Head Neck Surg. 2008 Feb;16(1):18-21. doi: 10.1097/MOO.0b013e3282f363f1.

Abstract

Purpose of review: This paper is a review of the most recent literature concerning the role of inflammatory genes in nasal polyposis. The data provide evidence of a pivotal role for some inflammatory mediators in the development and maintenance of nasal polyps.

Recent findings: Nasal polyposis is a common disease of the nasal mucosa; the exact mechanisms leading its development are still unknown. The role of the immune system in the pathogenesis of this disease is poorly understood. This lack of understanding makes definitive treatment very difficult. Activated eosinophils are a prominent feature of nasal polyps. Their presence in tissue results from a complex series of events that regulates their influx from the vasculature, as well as their movement, activation and survival within the tissue. Several studies have demonstrated that there are many potent chemoattractants that can activate eosinophils and trigger the inflammatory response.

Summary: Cytokines, chemokines and growth factors play an important role in the persistence of mucosal inflammation associated with nasal polyps. Metalloproteinases seem to be crucial in nasal tissue remodeling in these patients. Arachidonic acid metabolites seem to be particularly important in the pathogenesis of nasal polyps in patients with aspirin hypersensitivity. We discuss the contribution of each one for the polyp formation.

Publication types

  • Review

MeSH terms

  • Aspirin / adverse effects
  • Chemokines / metabolism
  • Cytokines / metabolism
  • Eosinophils / immunology
  • Gene Expression
  • Humans
  • Inflammation / genetics*
  • Inflammation / immunology*
  • Intercellular Signaling Peptides and Proteins / metabolism
  • Metalloproteases / metabolism
  • Nasal Polyps / genetics*
  • Nasal Polyps / immunology*

Substances

  • Chemokines
  • Cytokines
  • Intercellular Signaling Peptides and Proteins
  • Metalloproteases
  • Aspirin