Type 2 helper T-cell-skewed immune profiles characterize chronic rhinosinusitis with nasal polyps (CRSwNP), but the state of the neutrophil activation signaling pathway in CRSwNP is unknown. The purpose of this study was to examine neutrophil activation pathways in the pathogenesis of CRSwNP.
The institutional review board approved the study in which tissue proteomes were compared between control (inferior turbinate) and CRSwNP (nasal polyps) (n = 10/group) using an aptamer-based proteomics array and confirmed by whole transcriptomic analysis. Protein expression was analyzed using Student’s t-test and Benjamini–Hochberg procedures followed by the application of Ingenuity Pathway, MetaCore, and Genemania bioinformatics analyses.
All the patients with CRSwNP (n = 10) had eosinophilic nasal polyps. Compared with controls, proteins associated with the TREM-1 neutrophil activation signaling pathway such as Calcineurin B, zeta chain-associated protein kinase of 70 kD (ZAP70), 14-3-3 protein theta, 14-3-3 protein zeta/delta, PKC-D, Interleukin (IL)-17B, IL-17B receptor, IL-23, and IL-1B were significantly decreased in CRSwNP. In contrast, tissue eosinophil count and eosinophil-associated proteins such as C-C motif chemokine 17, periostin, and galectin ten significantly increased CRSwNP. Furthermore, the FC of the studied proteins’ expression was significantly correlated with their mRNA expression.
The study concluded that TREM-1-associated neutrophilic signaling pathway proteins are significantly suppressed in eosinophilic CRSwNP.
Reference: https://journals.sagepub.com/doi/full/10.1177/1945892418782233
