Cytokine Signature and Involvement in Chronic Rhinosinusitis with Nasal Polyps

Abstract

Cytokines are well known to play a central role in chronic rhinosinusitis with nasal polyps (CRSwNP), particularly in maintenance of the inflammatory response and the recruitment of eosinophils. The pathophysiological concepts concerning the involvement of inflammatory cytokines in CRSwNP have gradually evolved. Although the Th2 cytokines environment associated with an eosinophilic infiltration has retained a central role in the genesis of polyps, the role of other cytokine subpopulations has also and more recently been detailed, leading to a specific and complex signature in CRSwNP. The purpose of this review is to summarize the current state of knowledge about the cytokine signature in CRSwNP, the role of cytokines in the pathogenesis of this disease and in the intercellular dialog between epithelial cells, fibroblasts and inflammatory cells. Knowledge of this precise cytokine signature in CRSwNP is fundamental in the perspective of potential targeting biotherapies.

Keywords: chronic rhinosinusitis; cytokines; epithelial cell; inflammation; interleukin; nasal polyps.

Figure 1

Summary of cytokines network involved in CRSwNP. OSM: oncostatin M; MBP: major basic protein; ECP: eosinophilic cationic protein; EDN: eosinophil-derived neurotoxin. Following an aggression of the nasal epithelium by S. aureus, Alternaria or allergens, a Th2 inflammatory response is induced by IL-1α, IL-33, IL-25, TSLP and TNFα. IL-6, IL-4, and IL-13 cause IgE production and mast cell degranulation, and IL-5 causes eosinophil activation and survival. These phenomena, associated with the action of OSM and TGF-β, lead to tissue remodeling characterized by alteration of the epithelium and fibrosis.