Abstract
Chronic rhinosinusitis with nasal polyposis (CRSwNP) represents a heterogeneous disorder that can be classified into either eosinophilic or noneosinophilic endotypes. However, the immunological mechanisms of each remain unclear. The purpose of the present study was to compare and analyze inflammatory signatures of eosinophilic CRSwNP (ECRSwNP) and noneosinophilic CRSwNP (NECRSwNP). Cytokine antibody array was used to identify inflammatory mediators that were differentially expressed among ECRSwNP, NECRSwNP, and control groups. Then, bioinformatics approaches were conducted to explore biological functions and signaling pathways. In addition, pairwise correlation analyses were performed among differential levels of inflammatory mediators and tissue eosinophil infiltration. The results showed that nine mediators were significantly up-regulated in ECRSwNP, including eotaxin-2, eotaxin-3, CCL18, IL-4, IL-5, IL-10, IL-12p70, IL-13, and IL-15. Bioinformatics analysis indicated that these mediators were mainly enriched in leukocyte chemotaxis and proliferation, JAK-STAT cascade, asthma, and Th1 and Th2 cell differentiation. Furthermore, seven mediators were identified to be significantly up-regulated in NECRSwNP, including CCL20, resistin, transforming growth factor (TGF)-β2, triggering receptor expressed on myeloid cells 1 (TREM-1), CD14, glucocorticoid-induced tumor necrosis factor receptor related protein (GITR), and lipocalin-2. These mediators were closely associated with LPS responses, neutrophil chemotaxis and migration, and IL-17 signaling pathway. In addition, pairwise correlation analyses indicated that differential levels of inflammatory mediators in ECRSwNP and NECRSwNP were broadly correlated with each other and with tissue eosinophil infiltration. In conclusion, we found that ECRSwNP and NECRSwNP exhibited different patterns of inflammatory signatures. These findings may provide further insights into heterogeneity of CRSwNP.
Highlights
Chronic rhinosinusitis with nasal polyposis (CRSwNP) is a complex inflammatory condition characterized by the presence of edematous masses of inflamed mucosa in the upper airways [1,2]
Seven mediators were identified to be significantly up-regulated in NECRSwNP when compared with eosinophilic CRSwNP (ECRSwNP) and controls (Figure 5A), including CCL20, resistin, transforming growth factor (TGF)-β2, triggering receptor expressed on myeloid cells 1 (TREM-1), CD14, glucocorticoid-induced tumor necrosis factor receptor related protein (GITR), and lipocalin-2 (Figure 6)
We found a total of seven inflammatory mediators to be significantly up-regulated in NECRSwNP compared with ECRSwNP and controls, including CCL20, resistin, transforming growth factor beta 2 (TGF-β2), TREM-1, CD14, GITR, and lipocalin-2
Summary
Chronic rhinosinusitis with nasal polyposis (CRSwNP) is a complex inflammatory condition characterized by the presence of edematous masses of inflamed mucosa in the upper airways [1,2]. CRSwNP has a considerable impact on patients’ quality of life and is associated with high cost of management and significant morbidity [3]. Eosinophilic inflammation has been recognized as a major pathologic hallmark of CRSwNP in Caucasians. Recent studies have indicated that over half of the patients with CRSwNP in East Asia exhibit noneosinophilic inflammation [4,5]. Due to this heterogeneity, CRSwNP can be divided into two distinct endotypes, namely eosinophilic CRSwNP (ECRSwNP) and noneosinophilic CRSwNP (NECRSwNP) [6,7]. The precise mechanisms that underlie the pathogenesis of these two endotypes are still largely unknown
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
