A rat model of adenoid hypertrophy constructed by using ovalbumin and lipopolysaccharides to induce allergy, chronic inflammation, and chronic intermittent hypoxia

医学 鼻腔给药 卵清蛋白 鼻粘膜 炎症 缺氧(环境) 内科学 免疫学 嗜酸性粒细胞 免疫球蛋白E 内分泌学 病理 免疫系统 哮喘 抗体 化学 有机化学 氧气
作者
Anqi Liu,Yixing Zhang,Yan Lin,Xuejun Li,Shuming Wang,Wenyan Pu,Xiuxiu Liu,Zhiyan Jiang,Zhen Xiao
出处
期刊:Animal models and experimental medicine [Wiley]
标识
DOI:10.1002/ame2.12396
摘要

Abstract Background Adenoid hypertrophy (AH) is a common pediatric disease that significantly impacts the growth and quality of life of children. However, there is no replicable and valid model for AH. Methods An AH rat model was developed via comprehensive allergic sensitization, chronic inflammation induction, and chronic intermittent hypoxia (CIH). The modeling process involved three steps: female Sprague–Dawley rats (aged 4–5 weeks) were used for modeling. Allergen sensitization was induced via intraperitoneal administration and intranasal provocation using ovalbumin (OVA); chronic nasal inflammation was induced through intranasal lipopolysaccharide (LPS) administration for sustained nasal irritation; CIH akin to obstructive sleep apnea/hypopnea syndrome was induced using an animal hypoxia chamber. Postmodel establishment, behaviors, and histological changes in nasopharynx‐associated lymphoid tissue (NALT) and nasal mucosa were assessed. Arterial blood gas analysis and quantification of serum and tissue levels of (interleukin) IL‐4 and IL‐13, OVA‐specific immunoglobulin E (sIgE), eosinophil cationic protein (ECP), tumor necrosis factor (TNF‐α), IL‐17, and transforming growth factor (TGF)‐β were conducted for assessment. The treatment group received a combination of mometasone furoate and montelukast sodium for a week and then was evaluated. Results Rats exhibited notable nasal symptoms and hypoxia after modeling. Histopathological analysis revealed NALT follicle hypertrophy and nasal mucosa inflammatory cell infiltration. Elevated IL‐4, IL‐13, IL‐17, OVA‐sIgE, ECP, and TNF‐α levels and reduced TGF‐β levels were observed in the serum and tissue of model‐group rats. After a week of treatment, the treatment group exhibited symptom and inflammatory factor improvement. Conclusion The model effectively simulates AH symptoms and pathological changes. But it should be further validated for genetic, immunological, and hormonal backgrounds in the currently used and other strains and species.
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