哮喘联盟

   摘要
   背景：金黄色葡萄球菌肠毒素B（SEB）是一种超抗原，是小鼠和人类慢性气道炎症的调节因子。但有关SEB与天然免疫系统相互调节的机制尚不清楚。本实验在卵清蛋白（OVA）诱导的小鼠过敏性气道炎症模型中研究SEB与天然免疫系统相互作用的机制。
   方法：在暴露于OVA+SE的IL-1R基因敲除小鼠中研究超抗原诱导的过敏性炎症。多色流式细胞仪用于分析气道和淋巴结炎症细胞谱。使用Luminex计数来评价淋巴结IL-4、IL-5、IL-10和IL-13的生成情况。
   结果：在野生型小鼠中，鼻腔内给予OVA+SEB能诱导肺部炎症，表现为嗜酸性粒细胞、T细胞和树突状细胞数量增加、Th2细胞因子生成增加和OVA特异性IgE增加。在暴露于OVA+SEB的IL-1R基因敲除小鼠中，CD4+细胞聚集和Th2细胞因子生成减少。然而，敲除IL-1R并不影响任何过敏性气道炎症的特征，如支气管嗜酸性粒细胞增多、OVA特异性IgE生成和杯状细胞化生。
   结论：本研究结果为在细菌超抗原存在的情况下，气道过敏症的发生机制提供了新观点。OVA-SEB诱导的哮喘特征（如支气管嗜酸性粒细胞增多、杯状细胞增生和OVA-特异性IgE生成和炎症性树突状细胞增加）不依赖于IL-1R。然而，IL-1R信号传导对于CD4细胞聚集和Th2细胞因子生成至关重要。
 

（林江涛 审校）
Allergy. 2013 Jan 25. doi: 10.1111/all.12102. [Epub ahead of print]

 

The adjuvant-like activity of staphylococcal enterotoxin B in a murine asthma model is independent of IL-1R signaling.
 
Krysko O, Maes T, Plantinga M, Holtappels G, Imiru R, Vandenabeele P, Joos G, Krysko DV,Bachert C.

Source
Upper Airway Research Laboratory, Department of Oto-Rhino-Laryngology, Ghent University, Ghent, Belgium.

Abstract 
BACKGROUND: Staphylococcal enterotoxin B (SEB) is a superantigen known to be a modulator of chronic airway inflammation in mice and humans, yet little is known about the mechanisms that regulate its interaction with the innate immune system. We investigated this mechanism in a murine model of allergic airway inflammation induced by OVA (ovalbumin) in the presence of SEB.
METHODS: Superantigen-induced allergic inflammation was studied in IL-1R knockout (KO) mice exposed to OVA+SEB. Multicolor flow cytometry was used to analyze the inflammatory cell profile in airways and lymph nodes. Production of IL-4, IL-5, IL-10, and IL-13 in lymph nodes was assessed by Luminex technology.
RESULTS: In wild-type mice, endonasal instillation of OVA+SEB induced a pulmonary inflammation, characterized by an increase in the number of eosinophils, T cells, and dendritic cells and in the production of Th2 cytokines and OVA-specific IgE. In IL-1R KO mice exposed to OVA+SEB, attraction of CD4+ cells and production of Th2 cytokines were reduced. However, knocking out IL-1R did not affect any of the features of allergic airway inflammation, such as bronchial eosinophilia, OVA-specific IgE production and goblet cell metaplasia. 
CONCLUSION: We provide new insights into the mechanisms of airways allergy development in the presence of bacterial superantigen. The asthma features induced by OVA+SEB, such as bronchial eosinophilia, goblet cell proliferation, production of OVA-specific IgE and increase in inflammatory dendritic cells, are IL-1R independent. Yet, IL-1R signaling is crucial for CD4 cell accumulation and Th2 cytokine production.
 

Allergy. 2013 Jan 25. doi: 10.1111/all.12102. [Epub ahead of print]