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Effects of sinonasal type 2 inflammation on gene expression in the olfactory bulb and olfactory epithelium

ABSTRACT: Eosinophilic chronic rhinosinusitis (ECRS) is characterized by type 2 inflammation and olfactory dysfunction. The underlying mechanism for olfactory dysfunction in patients with ECRS remains to be elucidated. Therefore, we investigated changes in the olfactory bulb (OB) and olfactory epithelium (OE) associated with sinonasal type 2 inflammation, using a murine model of ECRS. We developed a murine model of ECRS based on the topical application of calcipotriol and ovalbumin for 14 days and subsequent daily intranasal challenge with ovalbumin for 5 days. Control mice received each treatment with the vehicles only. Mice were sacrificed on day 19. For RNA extraction, the OE and OB were micro-dissected, minced, and homogenized in TRIzol reagent. RNA-seq was performed to determine the impact of sinonasal type 2 inflammation on the OB and OE. RNA-seq revealed significant decrease in the gene expression levels of lipocalin family molecules in both OB and OE. These changes may be involved in the pathogenesis of olfactory dysfunction in ECRS.

ORGANISM(S): Mus musculus

PROVIDER: GSE310844 | GEO | 2026/09/01

REPOSITORIES: GEO

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Project description:Background: Allergic rhinitis (AR) is a global health burden affecting 20% of the pediatric population and is characterized by nasal inflammation and frequent olfactory dysfunction. Protein acetylation, which is a frequently occurring posttranslational modification, plays pivotal roles in the regulation of olfactory bulb (OB) function. However, the role of lysine acetylation in OB pathophysiology in pediatric AR-induced olfactory dysfunction remains unexplored. Methods: In this cross-sectional study, we enrolled pediatric patients (7–18 years) diagnosed with AR and age-matched healthy controls from the Children's Hospital affiliated with the Capital Institute of Pediatrics. Olfaction was assessed using the Universal Sniff (U-Sniff) test. An ovalbumin-induced AR mouse model was established. Olfactory function was assessed via buried food and odor discrimination tests. Proteomic and acetylomic profiling of OB tissue was performed using LC‒MS/MS, with bioinformatic analyses (GO, KEGG, STRING PPI, Motif). Key acetylation enzymes were validated by immunohistochemistry. Results: A total of 162 children in the AR and healthy groups were included in this study. A decreased score on “U-Sniff” and a greater incidence of olfactory dysfunction were observed in the AR group than in the healthy group (p<0.0001). AR model mice presented severe nasal symptoms, elevated sIgE levels, and significant olfactory deficits in odor detection and discrimination. Proteomic results revealed that the expression of proteins involved in glycolysis/gluconeogenesis and propanoate metabolism was significantly dysregulated. Critically, we observed dysregulation of key acetylation-modifying enzymes, characterized by reduced expression of the acetyl-CoA generator ACSS2 and deacetylase SIRT1, alongside elevated levels of acetyltransferase P300 and deacetylase HDAC2. Global acetylome profiling revealed 3,875 lysine acetylation sites across 1,707 proteins, indicating predominant hyperacetylation (436 significantly upregulated sites on 319 proteins versus 42 downregulated sites). These acetylated proteins disrupted olfactory transduction, the synaptic vesicle cycle, the citrate cycle (TCA cycle), glycolysis/gluconeogenesis, and propanoate metabolism. Our findings provide critical insights into how nasal inflammatory processes disrupt protein acetylation networks in the olfactory bulb, advancing our understanding of the molecular basis for smell disorders in children and informing future targeted interventions.

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Effects of sinonasal type 2 inflammation on gene expression in the olfactory bulb and olfactory epithelium

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