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过敏性肺部炎症小鼠模型的特征描述。

Characterization of a murine model of allergic pulmonary inflammation.

作者信息

Kung T T, Jones H, Adams G K, Umland S P, Kreutner W, Egan R W, Chapman R W, Watnick A S

机构信息

Schering-Plough Research Institute, Kenilworth, NJ 07033-0539.

出版信息

Int Arch Allergy Immunol. 1994 Sep;105(1):83-90. doi: 10.1159/000236807.

DOI:10.1159/000236807
PMID:8086833
Abstract

Pulmonary inflammation with eosinophil (EOs) infiltration is a prominent feature of allergic respiratory diseases such as asthma. In order to study the cellular response during the disease development, an animal model of IgE-mediated pulmonary inflammation with characteristic eosinophilia is needed. We developed a method for inducing severe pulmonary eosinophilia in the mouse and also studied the numbers of EOs in blood and bone marrow and the response to corticosteroid treatment. Animals were sensitized with alum-precipitated ovalbumin (OVA) and challenged with aerosolized OVA 12 days later when serum IgE levels were significantly elevated. Four to eight hours after challenge there were moderate increases in the number of EOs in the bone marrow and peripheral blood, but only a few EOs were observed in the lung tissue and in bronchoalveolar lavage (BAL) fluid. Twenty-four hours after challenge, there was a marked reduction of EOs in bone marrow, while the number of EOs peaked in the perivascular and peribronchial regions of the lung. Forty-eight hours after challenge, the highest number of EOs was found in the BAL fluid, making up > 80% of all cells in that compartment. The high levels of EOs in the lung tissue and BAL fluid lasted for 2-3 days and was followed by a more moderate but persistent eosinophilia for another 10 days. Nonsensitized animals showed no significant changes in the number of EOs in BAL fluid, lungs, blood or bone marrow. Histopathological evaluation also revealed epithelial damage, excessive mucus in the lumen and edema in the submucosa of the airways.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

嗜酸性粒细胞(EOs)浸润引起的肺部炎症是哮喘等过敏性呼吸道疾病的一个显著特征。为了研究疾病发展过程中的细胞反应,需要一种具有特征性嗜酸性粒细胞增多的IgE介导的肺部炎症动物模型。我们开发了一种在小鼠中诱导严重肺部嗜酸性粒细胞增多的方法,并研究了血液和骨髓中EOs的数量以及对皮质类固醇治疗的反应。用明矾沉淀的卵清蛋白(OVA)使动物致敏,12天后当血清IgE水平显著升高时,用雾化OVA进行激发。激发后4至8小时,骨髓和外周血中的EOs数量适度增加,但在肺组织和支气管肺泡灌洗(BAL)液中仅观察到少量EOs。激发后24小时,骨髓中的EOs数量显著减少,而肺的血管周围和支气管周围区域的EOs数量达到峰值。激发后48小时,BAL液中发现的EOs数量最多,占该区域所有细胞的80%以上。肺组织和BAL液中的高水平EOs持续2至3天,随后在另外10天内出现较为中度但持续的嗜酸性粒细胞增多。未致敏动物的BAL液、肺、血液或骨髓中的EOs数量无显著变化。组织病理学评估还显示气道上皮损伤、管腔内黏液过多和黏膜下水肿。(摘要截短至250字)

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