Lopuhaä C E, Out T A, Jansen H M, Aalberse R C, van der Zee J S
Department of Pulmonology, Academic Medical Center, Amsterdam, The Netherlands.
Clin Exp Allergy. 2002 Dec;32(12):1720-7. doi: 10.1046/j.1365-2222.2002.01542.x.
It is presently unknown which factors determine the occurrence and persistence of asthma in house dust mite-allergic individuals. The level of allergen-specific IgE antibodies does not seem to be decisive for asthmatic symptoms. Moreover, levels of exposure to mite allergens do not seem to differ significantly between asthmatic and non-asthmatics individuals.
It was hypothesized that the presence or absence of asthmatic symptoms in house dust mite-allergic patients is associated with quantitative or qualitative differences in the cellular bronchial inflammatory response during the late phase of the allergic reaction. This hypothesis was tested in the bronchial allergen challenge model.
Whole lung challenges with house dust mite extract were performed in 52 house dust mite-allergic subjects, of whom 26 had asthma and 26 had perennial rhinitis without asthmatic symptoms. Primary outcomes were parameters for bronchial inflammation in serial samples of induced sputum (cell differentials, eosinophil cationic protein (ECP), interleukin-8 (IL-8), myeloperoxydase (MPO)). In addition, lung function, non-specific bronchial hyper-responsiveness and serial blood samples (eosinophils and IL-5) were analysed.
At baseline sputum eosinophils and ECP were similar in both groups but neutrophils and IL-8 were higher in asthmatics. The early bronchoconstriction after allergen challenge was similar in asthma and non-asthmatic rhinitis (median decrease in FEV1: asthma -31.7% vs. non-asthmatics -29.1%, P > 0.1). The late phase bronchoconstriction was significantly greater in asthma (median decrease in FEV1: asthma -27.6% vs. non-asthmatics -18.9%, P = 0.02). Induction of bronchial hyper-responsiveness was similar in both groups. Bronchial allergen challenge elicited significant increases in sputum eosinophils and ECP, which were indistinguishable for both groups (P > 0.1 and P = 0.07, respectively). In contrast, higher numbers of neutrophils persisted in asthma 24h after challenge and were accompanied by significant increases in IL-8 and MPO, which were absent in non-asthmatics (difference between groups P = 0.007 and P = 0.05, respectively).
Allergen challenge inducedvery similar increases in eosinophils and ECP in induced sputum in allergic asthmatics and in allergic non-asthmatic patients. The difference in bronchial inflammation between asthma and non-asthmatic rhinitis appeared to be more closely related to indices for neutrophilic inflammation.
目前尚不清楚哪些因素决定了屋尘螨过敏个体哮喘的发生和持续存在。过敏原特异性IgE抗体水平似乎并非哮喘症状的决定性因素。此外，哮喘患者与非哮喘患者接触螨过敏原的水平似乎没有显著差异。
据推测，屋尘螨过敏患者哮喘症状的有无与过敏反应后期支气管细胞炎症反应的数量或质量差异有关。该假设在支气管过敏原激发模型中进行了检验。
对52名屋尘螨过敏受试者进行了全肺屋尘螨提取物激发试验，其中26人患有哮喘，26人患有常年性鼻炎但无哮喘症状。主要观察指标为诱导痰连续样本中的支气管炎症参数（细胞分类、嗜酸性粒细胞阳离子蛋白（ECP）、白细胞介素-8（IL-8）、髓过氧化物酶（MPO））。此外，还分析了肺功能、非特异性支气管高反应性和连续血样（嗜酸性粒细胞和IL-5）。
基线时，两组痰嗜酸性粒细胞和ECP相似，但哮喘患者的中性粒细胞和IL-8更高。过敏原激发后的早期支气管收缩在哮喘患者和非哮喘性鼻炎患者中相似（第一秒用力呼气容积（FEV1）中位数下降：哮喘患者为-31.7%，非哮喘患者为-29.1%，P>0.1）。哮喘患者的后期支气管收缩明显更大（FEV1中位数下降：哮喘患者为-27.6%，非哮喘患者为-18.9%，P=0.02）。两组支气管高反应性的诱导相似。支气管过敏原激发引起痰嗜酸性粒细胞和ECP显著增加，两组之间无明显差异（分别为P>0.1和P=0.07）。相比之下，哮喘患者在激发后24小时仍有较多的中性粒细胞，并伴有IL-8和MPO的显著增加，而非哮喘患者则没有（两组之间的差异分别为P=0.007和P=0.05）。
过敏原激发在过敏性哮喘患者和过敏性非哮喘患者的诱导痰中引起嗜酸性粒细胞和ECP非常相似的增加。哮喘与非哮喘性鼻炎之间的支气管炎症差异似乎与中性粒细胞炎症指标更为密切相关。
