Cockroach allergens induce biphasic asthma-like pulmonary inflammation in outbred mice.
Cockroach allergens induce biphasic asthma-like pulmonary inflammation in outbred mice.
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DOI：
10.3109/02770903.2012.678958
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发表时间：
2012-06
期刊：
影响因子：
--
通讯作者：
Remick DG
中科院分区：
文献类型：
--
作者：
Vaickus LJ;Bouchard J;Kim J;Natarajan S;Remick DG
本研究的目的是确定蟑螂过敏原（CRA）致敏和激发的远交种小鼠肺部炎症反应的动力学。在不使用佐剂的情况下，三次肺部暴露于CRA诱导哮喘样肺部炎症。在多个时间点处死小鼠，量化哮喘样肺部炎症。几个肺参数显示明显的双期炎症反应，早期（攻毒后1.5小时）和晚期（24小时）。初始阶段的特征是多种炎症介质的产生，包括CXC趋化因子，以及中性粒细胞向肺的募集。肺嗜酸性粒细胞的数量在早期减少，但很快反弹。除了气道高反应性外，早期和晚期均有TNF生成增加。该模型还显示早期产生粘蛋白并在12小时内清除，随后在肺上皮细胞中积累新的粘蛋白。肺内的Eotaxins在大约12小时达到峰值，在整个48小时的研究中，肺内嗜酸性粒细胞的数量保持不变。对临床相关过敏原反应的肺部炎症参数定义了双期反应。这些数据可用于研究疾病的发病机制和开发针对不同阶段的靶向治疗。
The aim of this study is to define the kinetics of the pulmonary inflammatory response in cockroach allergen (CRA) sensitized and challenged outbred mice. Asthma-like pulmonary inflammation was induced with three pulmonary exposures to CRA, without the use of adjuvants. Mice were sacrificed at multiple time points and asthma-like pulmonary inflammation quantified. Several pulmonary parameters showed a pronounced biphasic inflammatory response with an early stage (1.5 hours post challenge) and late stage (24 hours). The initial phase was characterized by the production of multiple inflammatory mediators, including CXC chemokines, and the recruitment of neutrophils to the lung. The number of pulmonary eosinophils decreased in the early phase but quickly rebounded. Both the early and late phases had increases in TNF production in addition to airways hyperreactivity. The model also demonstrated early production of mucin with clearance by 12 hours followed by new accumulation of mucin in the pulmonary epithelial cells. Eotaxins within the lung peaked at about 12 hours and the numbers of eosinophils in the lung remained constant throughout the 48 hours of the study. The pulmonary inflammatory parameters in response to a clinically relevant allergen define a biphasic response. These data may be used to investigate the pathogenesis of the disease and develop targeted therapies for the distinct phases.
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影响因子：
14.2
作者：
FREW, AJ;KAY, AB
通讯作者：
KAY, AB
影响因子：
3.4
作者：
Barnes, PJ
通讯作者：
Barnes, PJ
影响因子：
5.8
作者：
Conroy DM;Williams TJ
通讯作者：
Williams TJ
DOI：
10.4049/jimmunol.0900634
发表时间：
2010-06-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Bates ME;Sedgwick JB;Zhu Y;Liu LY;Heuser RG;Jarjour NN;Kita H;Bertics PJ
通讯作者：
Bertics PJ
影响因子：
14.2
作者：
Choi, IW;Sun-Kim;Lee, HK
通讯作者：
Lee, HK