内源性哮喘患者痰液中出现功能性尘螨特异性IgE
2011/06/17
摘要
原理：Rackeman将内源性哮喘描述为无过敏的哮喘。研究发现，内源性哮喘患者局部存在IgE的产生，但该反应的抗原特异性尚待澄清。
目的：研究（1）内源性哮喘患者痰液尘螨特异性IgE；（2）该IgE的临床/免疫相关性；（3）该IgE的功能。
方法：对来自于内源性哮喘患者、过敏性哮喘患者和对照者的痰液，采用ELISA检测屋尘螨(Der p)和其重组主要过敏原(rDer p1和rDer p2)的特异性IgE。采用Der p进行全肺激发试验，观察临床和炎症指标。通过嗜碱性粒细胞（表面表达CD203c）活化试验，检测局部IgE刺激效应细胞的能力。
检测指标和主要结果：与健康非过敏症者相比，内源性哮喘患者的总IgE和Der p特异性IgE水平增加。在Der p暴露后，内源性哮喘患者未观察到即刻的哮喘反应。痰液Der p特异性IgE能识别主要的过敏原Der p1和Der p2，而且能活化过敏症患者血液中的嗜碱性粒细胞。
结论：内源性哮喘患者痰液中存在IgE，这些IgE能识别Der p过敏原。尽管这些IgE对主要的过敏原具有特异性，而且在体外能活化效应细胞，但该IgE的反应性与Der p暴露后的反应无临床相关性。我们认为，内源性哮喘患者缺少通过FcεRI促进IgE介导的哮喘反应的二级信号。
（林江涛 审校）
Am J Respir Crit Care Med. 2011 Apr 7. [Epub ahead of print]
Presence in Sputum of Functional Dust Mite-specific IgE Antibodies in Intrinsic Asthma.
Mouthuy J, Detry B, Sohy C, Pirson F, Pilette C.
Pneumology, Cliniques universitaires St-Luc, Brussels, Belgium; Université catholique de Louvain (UCL), Institut de Recherche Expérimentale et Clinique (IREC), pôle Pneumologie, ORL & Dermatologie, Brussels, Belgium.
Abstract
RATIONALE: Intrinsic asthma was described by Rackeman as asthma without allergy. Local IgE production has been documented in intrinsic asthma, but antigen specificity of this response remains elusive.
OBJECTIVES: We investigated (1) the presence of dust mite-specific IgE in sputum of intrinsic asthmatics, (2) their clinical/immunological relevance and (3) their functionality.
METHODS: Specific IgE to Dermatophagoïdes pternonyssinus (Der p) and to recombinant major allergens (rDer p1 and rDer p2) were assayed by ELISA in sputum samples from intrinsic vs atopic asthmatics and controls. Whole-lung challenge was performed with Der p, for clinical and inflammatory readouts. Functionality of local IgE to trigger effector cells was assessed using basophil activation test (surface expression of CD203c).
MEASUREMENTS AND MAIN RESULTS: Both total IgE and Der p-specific IgE levels are increased in intrinsic asthma patients compared to healthy nonatopics. However, no immediate asthmatic responses were observed in intrinsic patients following Der p exposure. These sputum Der p-specific IgE do however recognize major allergens Der p1 and Der p2, and are able to trigger activation of blood basophils from atopic donor.
CONCLUSION: We confirm that IgE production occurs in intrinsic asthma, and show that part of this IgE recognizes Der p antigens. However, this IgE reactivity does not translate into clinical responses to Der p exposure, despite specificity to major allergens and functionality to activate effector cells in vitro. We postulate that a second signal that promotes IgE-mediated asthmatic responses through FcεRI is lacking in intrinsic asthma.
Am J Respir Crit Care Med. 2011 Apr 7. [Epub ahead of print]
原理：Rackeman将内源性哮喘描述为无过敏的哮喘。研究发现，内源性哮喘患者局部存在IgE的产生，但该反应的抗原特异性尚待澄清。
目的：研究（1）内源性哮喘患者痰液尘螨特异性IgE；（2）该IgE的临床/免疫相关性；（3）该IgE的功能。
方法：对来自于内源性哮喘患者、过敏性哮喘患者和对照者的痰液，采用ELISA检测屋尘螨(Der p)和其重组主要过敏原(rDer p1和rDer p2)的特异性IgE。采用Der p进行全肺激发试验，观察临床和炎症指标。通过嗜碱性粒细胞（表面表达CD203c）活化试验，检测局部IgE刺激效应细胞的能力。
检测指标和主要结果：与健康非过敏症者相比，内源性哮喘患者的总IgE和Der p特异性IgE水平增加。在Der p暴露后，内源性哮喘患者未观察到即刻的哮喘反应。痰液Der p特异性IgE能识别主要的过敏原Der p1和Der p2，而且能活化过敏症患者血液中的嗜碱性粒细胞。
结论：内源性哮喘患者痰液中存在IgE，这些IgE能识别Der p过敏原。尽管这些IgE对主要的过敏原具有特异性，而且在体外能活化效应细胞，但该IgE的反应性与Der p暴露后的反应无临床相关性。我们认为，内源性哮喘患者缺少通过FcεRI促进IgE介导的哮喘反应的二级信号。
（林江涛 审校）
Am J Respir Crit Care Med. 2011 Apr 7. [Epub ahead of print]
Presence in Sputum of Functional Dust Mite-specific IgE Antibodies in Intrinsic Asthma.
Mouthuy J, Detry B, Sohy C, Pirson F, Pilette C.
Pneumology, Cliniques universitaires St-Luc, Brussels, Belgium; Université catholique de Louvain (UCL), Institut de Recherche Expérimentale et Clinique (IREC), pôle Pneumologie, ORL & Dermatologie, Brussels, Belgium.
Abstract
RATIONALE: Intrinsic asthma was described by Rackeman as asthma without allergy. Local IgE production has been documented in intrinsic asthma, but antigen specificity of this response remains elusive.
OBJECTIVES: We investigated (1) the presence of dust mite-specific IgE in sputum of intrinsic asthmatics, (2) their clinical/immunological relevance and (3) their functionality.
METHODS: Specific IgE to Dermatophagoïdes pternonyssinus (Der p) and to recombinant major allergens (rDer p1 and rDer p2) were assayed by ELISA in sputum samples from intrinsic vs atopic asthmatics and controls. Whole-lung challenge was performed with Der p, for clinical and inflammatory readouts. Functionality of local IgE to trigger effector cells was assessed using basophil activation test (surface expression of CD203c).
MEASUREMENTS AND MAIN RESULTS: Both total IgE and Der p-specific IgE levels are increased in intrinsic asthma patients compared to healthy nonatopics. However, no immediate asthmatic responses were observed in intrinsic patients following Der p exposure. These sputum Der p-specific IgE do however recognize major allergens Der p1 and Der p2, and are able to trigger activation of blood basophils from atopic donor.
CONCLUSION: We confirm that IgE production occurs in intrinsic asthma, and show that part of this IgE recognizes Der p antigens. However, this IgE reactivity does not translate into clinical responses to Der p exposure, despite specificity to major allergens and functionality to activate effector cells in vitro. We postulate that a second signal that promotes IgE-mediated asthmatic responses through FcεRI is lacking in intrinsic asthma.
Am J Respir Crit Care Med. 2011 Apr 7. [Epub ahead of print]
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