Sensitization to Inhaled Ryegrass Pollen by Collateral Priming in a Murine Model of Allergic Respiratory Disease
Sensitization to Inhaled Ryegrass Pollen by Collateral Priming in a Murine Model of Allergic Respiratory Disease
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过敏性呼吸道疾病小鼠模型中通过并行启动对吸入黑麦草花粉致敏
DOI:
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发表时间:
2010
影响因子:
2.8
通讯作者:
J. Ceuppens
中科院分区:
文献类型:
--
作者:
P. Cadot;I. Meyts;J. Vanoirbeek;B. Vanaudenaerde;D. Bullens;J. Ceuppens
Background: Mouse models of asthma suffer from the necessity to prime the animals by injections before respiratory exposure. Our aim was to develop a mouse model that mimics the progression of human allergic disease upon low-dose inhaled allergen exposure. Methods: Mice were primed intraperitoneally to ovalbumin (OVA) before they were exposed repeatedly to aerosols of either OVA, ryegrass (Lolium perenne) pollen extract, or both concomitantly. The sensitization to ryegrass pollen proteins was evaluated by measurement of specific serum antibody, by the respiratory response to a challenge with ryegrass pollen extract and by lung cytokine production after challenge. Results: Inhalation of ryegrass pollen extract alone did not result in sensitization. Sensitization to inhaled ryegrass pollen proteins, however, did occur in mice that had been sensitized to OVA by intraperitoneal injections and were then exposed to inhaled ryegrass pollen extract and OVA simultaneously. T and B cell priming was ascertained by ryegrass pollen-specific IgG1 and IgE antibody production and by induction of airway inflammation and of Th2 cytokine mRNA transcripts in the lungs upon airway challenge with ryegrass pollen extract. A progressive spread of the IgE/IgG1 response to different ryegrass pollen proteins could be visualized in immunoblots by comparing antibody patterns at day 56 and 86. Conclusions: Low-dose inhalatory allergen exposure results in sensitization when airways are exposed at the same time to another allergen to which the animals are already sensitized. This model can help to unravel the mechanisms that underlie the development and progression of respiratory allergic diseases.
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DOI:
10.1164/ajrccm.156.3.9606031
发表时间:
1997-09-01
影响因子:
24.7
作者:
Hamelmann, E;Schwarze, J;Gelfand, EW
通讯作者:
Gelfand, EW
DOI:
10.4049/jimmunol.174.9.5864
发表时间:
2005
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Hayashi,Tomoko;Gong,Xing;Rossetto,Cyprian;Shen,Carol;Takabayashi,Kenji;Redecke,Vanessa;Spiegelberg,Hans;Broide,David;Raz,Eyal
通讯作者:
Raz,Eyal
影响因子:
4.4
作者:
Manca,F;Seravalli,E;Valle,MT;Fenoglio,D;Kunkl,A;LiPira,G;Zolla-Pazner,S;Celada,F
通讯作者:
Celada,F
影响因子:
14.2
作者:
Goplen, Nicholas;Karim, Zunayet;Liang, Qiaoling;Gorska, Magdalena M.;Rozario, Sadee;Guo, Lei;Alam, Rafeul
通讯作者:
Alam, Rafeul