ArticleInternational forum of allergy & rhinology2016
Characterization of a novel high-dose ovalbumin-induced murine model of allergic sinonasal inflammation.
Article in International forum of allergy & rhinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 15 citations in OpenAlex.
- Lipocalin 2 deficiency impacts angiogenesis after ischemia in vivo and in vitro.Vascular biology (Bristol, England) · 2025Article
- Deletion of Nrf2 enhances susceptibility to eosinophilic sinonasal inflammation in a murine model of rhinosinusitis.International forum of allergy & rhinology · 2019Article
- Characterization of a novel, papain-inducible murine model of eosinophilic rhinosinusitis.International forum of allergy & rhinology · 2018Article
- Airborne Particulate Matter Induces Nonallergic Eosinophilic Sinonasal Inflammation in Mice.American journal of respiratory cell and molecular biology · 2017Article
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6 authors at 1 institution in 1 country.
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Abstract
backgroundFew efficacious topical therapies exist for chronic rhinosinusitis (CRS). The lack of a reproducible mouse model of CRS limits the pilot testing of potential novel anti-inflammatory therapies. Although the ovalbumin-induced mouse model of sinonasal inflammation is commonly used, it is difficult to reproduce and can generate variable histologic results. In this study, we explore a variation of this model in different strains of mice and explore various inflammatory cytokines as reproducible molecular markers of inflammation.
methodsAllergic sinonasal inflammation was generated in BALB/c and C57BL/6 mice using intraperitoneal high-dose injections of ovalbumin (Ova; Sigma Chemical Co.) followed by 10 days of high-dose intranasal sensitization. Real-time polymerase chain reaction (RT-PCR) for eotaxin, interleukin 4 (IL-4), and IL-13 were measured from sinonasal mucosa. We also pilot tested a known topical budesonide to characterize the anti-inflammatory response. Histological sections were analyzed for epithelial thickness and eosinophilia.
resultsBoth BALB/c and C57BL/6 mice consistently showed increases in T helper 2 (Th2) cytokines after sensitization with high-dose Ova (p < 0.0001) when compared to controls. There were also significant increases in epithelial thickening in Ova-sensitized mice and eosinophilia in both BALB/c and C57BL/6 strains. In addition, topical budesonide significantly reduced anti-inflammatory cytokines, eosinophilia, and epithelial thickness.
conclusionOur variation of the ovalbumin-induced mouse model of sinonasal inflammation in both BALB/c and C57BL/6 mice provides an efficacious model for testing potential topical anti-inflammatory therapies for CRS. The utilization of sinonasal mucosal Th2 cytokines along with histologic markers provides a consistent and quantifiable marker of inflammation in assessing the efficacy of candidate drugs.
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