受体相互作用蛋白 2（RIP2）在卵清蛋白诱导的小鼠气道炎症中是可有可无的。
Receptor Interacting Protein 2 (RIP2) Is Dispensable for OVA-Induced Airway Inflammation in Mice.
机构信息
Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University, Seoul, Korea.
Department of Microbiology and Immunology, School of Medicine, Pusan National University, Yangsan, Korea.
出版信息
Allergy Asthma Immunol Res. 2014 Mar;6(2):163-8. doi: 10.4168/aair.2014.6.2.163. Epub 2013 Oct 30.
PURPOSE
Asthma is a pulmonary chronic inflammatory disease characterized by airway obstruction and hyperresponsiveness. Pattern recognition receptors are known to play a key role in the development of allergic diseases as well as host defenses against microbial infection. Receptor interacting protein 2 (RIP2), a serine/threonine kinase, is an adaptor molecule of NOD1 and NOD2, and genetic variation in this receptor is known to be associated with the severity of allergic asthma in children. In this study, we examined the role of RIP2 in the development of allergic airway inflammation in a mouse model.
METHODS
Airway inflammation was induced in mice through intranasal administration of ovalbumin (OVA) after 2 intraperitoneal immunizations with OVA. Lung inflammation and mucus hypersecretion were examined histologically and total cell infiltration in bronchoalveolar (BAL) fluids was determined. Levels of the Th2-related cytokines, IL-5 and IL-13, in lung extracts were measured by ELISA. Serum antigen-specific IgE and IgG1 levels were also assessed.
RESULTS
OVA-induced lung inflammation and mucus hypersecretion were not different between WT and RIP2-deficient mice. The IL-5 and IL-13 levels in the bronchoalveolar (BAL) fluids were also not impaired in RIP2-deficient mice compared to WT mice. Moreover, RIP2 deficiency did not affect serum OVA-specific IgG1 and IgE levels.
CONCLUSIONS
Our results suggest that RIP2 is not associated with the development of allergic airway inflammation.
目的
哮喘是一种肺部慢性炎症性疾病，其特征为气道阻塞和高反应性。模式识别受体在过敏性疾病的发展以及宿主对微生物感染的防御中起着关键作用。受体相互作用蛋白 2（RIP2）是一种丝氨酸/苏氨酸激酶，是 NOD1 和 NOD2 的衔接分子，该受体的遗传变异与儿童过敏性哮喘的严重程度有关。在本研究中，我们研究了 RIP2 在小鼠过敏性气道炎症模型中的作用。
方法
通过用卵清蛋白（OVA）对小鼠进行两次腹腔免疫后，经鼻内给予 OVA 诱导气道炎症。通过组织学检查评估肺炎症和黏液分泌过度，通过测定支气管肺泡（BAL）液中的总细胞浸润来确定。通过 ELISA 测定肺提取物中 Th2 相关细胞因子 IL-5 和 IL-13 的水平。还评估了血清抗原特异性 IgE 和 IgG1 水平。
结果
OVA 诱导的肺炎症和黏液分泌过度在 WT 和 RIP2 缺陷型小鼠之间没有差异。与 WT 小鼠相比，RIP2 缺陷型小鼠的支气管肺泡（BAL）液中的 IL-5 和 IL-13 水平也没有受损。此外，RIP2 缺陷对血清 OVA 特异性 IgG1 和 IgE 水平没有影响。
结论
我们的结果表明 RIP2 与过敏性气道炎症的发展无关。
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