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.
Highlights
Chronic rhinosinusitis with nasal polyps (CRSwNP) or without nasal polyps (CRSsNP)are inflammatory diseases of the nasal mucosa and paranasal sinuses
IL-1α, considered as an alarmin and IL-1β, which is processed by the inflammasome, are immunoregulatory proteins secreted by activated monocytes, macrophages, natural killer cells, epithelial cells and fibroblasts, and they activate upstream the cascade of the inflammation process via a shared receptor [77]
In CRSwNP, IL-6 messenger ribonucleic acid (mRNA) and protein are overexpressed in nasal polyps compared to normal mucosa [87], probably by fibroblasts able to modulate the activation of immune responses and the synthesis of stroma
Summary
Chronic rhinosinusitis with nasal polyps (CRSwNP) or without nasal polyps (CRSsNP). are inflammatory diseases of the nasal mucosa and paranasal sinuses. The cytokines produced by these immune cells and a number of other cells (epithelial cells or fibroblasts) play a central role in the pathogenesis of inflammatory diseases, including CRSwNP. The concept of endotype progressively emerged and was defined according to the cytokines signature found in different group of patients: (a) markers of eosinophilic and Th2 driven inflammation, (b) neutrophilic and proinflammatory cytokines, (c) Th17- or Th22related markers and (d) Th1 inflammatory markers. Cytokines play a central and essential role in the genesis of CRSwNP, in the maintenance of the inflammatory response and the recruitment of eosinophils. 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. T lymphocytes, natural killer, monocytes, dendritic cells, endothelial, epithelial cells and fibroblasts
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
