Abstract

A receptor for advanced glycation end products (RAGE) and its ligand high mobility group box 1 (HMGB1) protein has been linked to several chronic diseases, and acts as a trigger for inflammation signaling. Here, we study RAGE and HMGB1 expression in chronic, recalcitrant rhinosinusitis with nasal polyps (CRSwNP) to determine its potential clinical significance, i.e., disease recurrence and severity. RAGE and HMGB1 expression in CRSwNP was evaluated by immunohistochemistry in epithelial cells of fresh sinonasal mucosa samples obtained from the patients diagnosed with recalcitrant CRSwNP (n = 25) and normal control mucosa (NC) (n = 26). RAGE and HMGB1 expression levels in tissues were correlated with disease severity assessed by nasal endoscopy, CT scan, number of previous sinus surgeries, allergy status and nasosinusal microbiology. RAGE and HMGB1 were moderately or strongly expressed in CRSwNP tissue. No or weak RAGE expression was found in NC. HMGB1 was equally strongly expressed in NC. We observed a strong correlation between RAGE and disease severity, recurrence, undergone operations, asthma and aspirin exacerbated respiratory disease (AERD). Elevated RAGE expression is associated with increased disease severity, as well as allergy and AERD in patients with recalcitrant CRSwNP. It is possible that the explanation for recurrent CRSwNP pathogenesis might be related to RAGE overexpression with subsequent sinus mucosa hyperproliferation, necessitating several operations.

Highlights

  • Recent studies suggest that the receptor for advanced glycation end products (RAGE) has been implicated in initiating and perpetuating inflammatory responses

  • Pathogenesis of CRSwNP is associated with aberrant innate or adaptive immune responses that may initially result from inappropriate expression of RAGE and high mobility group box 1 (HMGB1) protein or/and responses to its signaling pathway

  • To address this hypothesis we sought to understand the role of RAGE in recalcitrant CRSwNPs pathogenesis and the manner in which RAGE interacts with its ligand HMGB1 in the sinonasal mucosa (SM)

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Summary

Introduction

Recent studies suggest that the receptor for advanced glycation end products (RAGE) has been implicated in initiating and perpetuating inflammatory responses. Due to an enhanced level of RAGE ligands in chronic disorders, this receptor is hypothesized to have a causative effect in a range of inflammatory diseases (Bassi et al 2008; Singh et al 2014). RAGE is a multiligand receptor and a member of the immunoglobulin superfamily of cell surface molecules which is found on smooth muscle cells, macrophages, endothelial cells and astrocytes. Its name comes from its ability to bind advanced glycation end products (AGE).

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