Large-scale gene expression profiling reveals distinct type 2 inflammatory patterns in chronic rhinosinusitis subtypes

Abstract

In an attempt to better classify molecular profiles in chronic rhinosinusitis (CRS)subtypes and promote endotyping, we characterize the expression of relevant type 2 inflammatory markers in several clinical subtypes of CRS.

Figure 1. Expression of canonical type 2 inflammatory markers in CRS subtypes

(A) Expression of IgE. Samples from each disease subtype are stratified according to presence or absence of asthma phenotype. (B) Relative expression of several canonical upstream regulators of type 1 (IFNG) or type 2 inflammation (IL-4, IL-5, IL-13) as measured by droplet digital PCR. (C and D) Relative expression of important downstream type 2 inflammatory gene clusters. †p<0.05, * p<0.01, ** p<0.001 for comparisons of HC vs each subtype. When no annotation is indicated, the comparison was not significant. POSTN - periostin

Figure 2. ILRL1 expression and mast cell activity in CRS

(A) Box and whisker plot of differential expression of IL1RL1 by microarray analysis. (B) Correlation of IL1RL1 and tryptase gene cluster. r2 = 0.46, p<0.001. (C and D) IL-33 expression, mast cell and eosinophil infiltration in representative CRSwNP tissue. (C) Representative photomicrograph illustrating IL-33 expression located in the nasal surface epithelium (black arrow) as well as the stroma (blue arrow) containing inflammatory infiltrate. (D) Photomicrographs demonstrating expression of IL-33 associated with varying levels of eosinophil and mast cell infiltration. MBP: major basic protein. ** p<0.001 for comparisons of HC vs each subtype. When no annotation is indicated, the comparison was not significant.