Erythromycin Reduces Nasal Inflammation by Inhibiting Immunoglobulin
Production, Attenuating Mucus Secretion, and Modulating Cytokine
Expressions: Evidence from Chronic Rhinosinusitis Model of Mice
Abstract
Background: Allergic rhinitis (AR) and chronic rhinosinusitis (CRS) are
common airway diseases worldwide. AR and CRS frequently occur together
in a patient, and they share some similar pathological mechanisms. The
aim of this study was to investigate the impact of AR on the
pathophysiology of CRS. In addition, we explored the efficacy of
erythromycin (EM) treatment on experimental CRS mice with or without AR
(CRSsAR, CRSwAR). Methods: Patient nasal tissues were obtained from
those underwent nasal surgery. Subjects were divided into three groups:
control, CRSsAR, and CRSwAR groups. Experimental mice were divided
similarly into control, CRSsAR, and CRSwAR groups. In addition, CRSsAR
and CRSwAR mice were treated with EM at 0.75, 7.5, or 75mg/kg or with
dexamethasone (Dex) at 1mg/kg. Results: Allergy exacerbates nasal
inflammation that was evident in nasal histology and cytokine
expressions both in patients and in mice with CRS. Dex 1 mg/kg, EM 7.5
or 75 mg/kg treatments all effectively inhibited nasal inflammation in
mice. EM reduced serum immunoglobulin levels, inhibited mucosal mucus
production, and modulated local cytokine expressions in CRS mice with or
without AR. Anti-inflammatory mechanisms of EM and of Dex did not appear
to be the same. EM showed inhibitions on immunoglobulin production and
mucus secretion stronger than Dex. Dex broadly reduced cytokine
expressions whereas EM had an immunomodulatory effect on Th1/Th2
cytokine expressions. Conclusions: Comorbid AR enhanced sinonasal
inflammation of CRS. EM and Dex treatments showed similar
anti-inflammatory effects on CRS but through partly different
mechanisms.