Periostin May Play a Protective Role in the Development of Eosinophilic Chronic Rhinosinusitis With Nasal Polyps in a Mouse Model
Periostin May Play a Protective Role in the Development of Eosinophilic Chronic Rhinosinusitis With Nasal Polyps in a Mouse Model
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DOI：
10.1002/lary.23786
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发表时间：
2013-05-01
期刊：
影响因子：
2.6
通讯作者：
Kim, Dae Woo
中科院分区：
文献类型：
--
作者：
Kim, Sang-Wook;Kim, Jin Hyun;Kim, Dae Woo
目的/假设：在之前的基因分析中，有报道称人类鼻息肉中有几个基因上调。在这些基因中，已知骨膜蛋白在阿司匹林敏感患者的鼻息肉中过度表达。使用骨膜素缺失小鼠，我们研究了骨膜素在伴有鼻息肉的嗜酸性鼻窦炎小鼠模型中的作用。研究设计：动物研究。方法：根据先前建立的方案，在骨膜素缺失小鼠和野生型小鼠中诱导嗜酸性鼻窦炎。简而言之，卵清蛋白（OVA）用于致敏和延长鼻内刺激。鼻内应用金黄色葡萄球菌肠毒素 B 以形成息肉样病变。为了检查炎症和粘膜病变，进行了苏木精和伊红、天狼星红和吉姆萨染色。结果：骨膜素缺失小鼠和野生型小鼠的最大粘膜厚度没有明显差异。相反，与野生型相比，骨膜蛋白缺失小鼠的一些炎症参数，包括息肉样病变和肥大细胞的数量，有所加重。与 OVA 刺激的野生型小鼠相比，OVA 刺激的骨膜素缺失小鼠的嗜酸性粒细胞浸润加剧，而用额外的金黄色葡萄球菌肠毒素 B 攻击的野生型和骨膜素缺失小鼠之间没有明显差异。结论：在伴有鼻息肉的嗜酸粒细胞性鼻窦炎小鼠模型中，骨膜素的丧失似乎增强了息肉样病变的形成和肥大细胞浸润。
Objectives/Hypothesis: Several genes have been reported to be upregulated in human nasal polyps in previous genetic analyses. Among these genes, periostin is known to be overexpressed in nasal polyps obtained from aspirin-sensitive patients. Using periostin-null mice, we investigated the role of periostin in a murine model of eosinophilic rhinosinusitis with nasal polyps.Study Design: Animal study.Methods: Eosinophilic rhinosinusitis was induced in both periostin-null and wild-type mice according to previously established protocols. In brief, ovalbumin (OVA) was used for sensitization and prolonged intranasal stimulation. Staphylococcus aureus enterotoxin B was applied intranasally to develop polyplike lesions. To examine the inflammation and mucosal lesions, hematoxylin and eosin, Sirius red, and Giemsa staining were performed.Results: There was no definite difference in the maximal mucosal thickness between periostin-null and wild-type mice. In contrast, some parameters of inflammation, including the number of polyplike lesions and mast cells, were aggravated in the periostin-null mice compared to wild type. Eosinophilic infiltration was aggravated in the OVA-stimulated periostin-null mice, compared to OVA-stimulated wild-type mice, whereas there was no apparent difference between wild-type and periostin-null mice challenged with additional S aureus enterotoxin B.Conclusions: The loss of periostin appears to enhance polyplike lesion formation and mast cell infiltration in a mouse model of eosinophilic rhinosinusitis with nasal polyps.