Differential expression of CCL18 in moderate/severe and mild persistent allergic rhinitis and its correlation with

Ashkan Pirayesh1, Samira Ferdosi2, Hedayatollah Shirzad1

  • 1a Cellular and Molecular Research Center, Basic Health Sciences Institute , Shahrekord University of Medical Sciences , Shahrekord , Iran.

Abstract

Insights

Chemokine ligand 18 (CCL-18) expression in nasal turbinates is elevated in moderate-to-severe persistent allergic rhinitis. Higher CCL-18 levels correlate with symptom severity and IgE in allergic rhinitis patients.

Area of Science:

  • Immunology
  • Otorhinolaryngology
  • Allergy Research

Background:

  • Persistent allergic rhinitis (PAR) is a common condition affecting nasal mucosa.
  • Understanding the molecular mechanisms underlying PAR severity is crucial for effective treatment.
  • Chemokine ligand 18 (CCL-18) is implicated in inflammatory processes.

Purpose of the Study:

  • To evaluate CCL-18 expression in nasal inferior turbinate mucosa of patients with mild (M) and moderate-to-severe (M/S) PAR.
  • To correlate CCL-18 levels with disease severity and immunological markers.

Main Methods:

  • Case-controlled study comparing M/S PAR, M PAR, and healthy controls.
  • Nasal inferior turbinate biopsies for CCL-18 mRNA analysis via real-time PCR.
  • Serum CCL-18 levels measured by ELISA; total and specific IgE levels assessed.
  • Clinical severity assessed using the total nasal syndrome score (TNSS).

Main Results:

  • Significantly increased CCL-18 mRNA expression and serum levels in M/S PAR patients compared to controls and M PAR patients.
  • CCL-18 serum levels positively correlated with TNSS in M/S PAR patients.
  • Statistical correlation observed between serum CCL-18 and total serum IgE levels.

Conclusions:

  • CCL-18 expression in nasal turbinate mucosa may be linked to the severity of persistent allergic rhinitis.
  • CCL-18 could serve as a potential biomarker for allergic rhinitis severity.
  • Further research is warranted to elucidate the role of CCL-18 in PAR pathogenesis.

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