Ying S, Humbert M, Meng Q, Pfister R, Menz G, Gould H J, Kay A B, Durham S R
Allergy and Clinical Immunology, Imperial College School of Medicine at the National Heart and Lung Institute, Dovehouse St., London SW3 6LY, UK.
J Allergy Clin Immunol. 2001 Apr;107(4):686-92. doi: 10.1067/mai.2001.114339.
The demonstration of epsilon germline gene (Cepsilon) transcripts and mature mRNA for the epsilon heavy chain gene (Iepsilon) in the nasal mucosa suggested that IgE synthesis may occur in allergic rhinitis.
In view of our previous demonstration of increases in IL-4 mRNA(+) cells in asthmatic subjects, we assessed whether local IgE synthesis may also be a feature of bronchial asthma.
Fiberoptic bronchoscopic mucosa biopsy specimens were obtained from 9 atopic asthmatic subjects and 10 nonatopic normal (intrinsic) control subjects. To control for atopy, we also studied 9 nonatopic asthmatic subjects and 10 atopic nonasthmatic control subjects. Tissue was processed for immunohistochemistry for B cells (CD20) and in situ hybridization for Iepsilon and Cepsilon RNA(+) cells and IL-4 mRNA(+) cells.
B-cell numbers in the bronchial mucosa were similar for asthmatic subjects compared with control subjects, whereas significantly higher numbers of Iepsilon RNA(+) (P =.02 and P =.04, respectively), Cepsilon RNA(+) (P =.01 and P =.03, respectively), and IL-4 mRNA(+) (P =.001 and P =.001, respectively) cells were observed in atopic asthmatic subjects and nonatopic asthmatic subjects, respectively, but not in atopic control subjects compared with nonatopic control subjects. In asthmatic subjects there were significant correlations between Iepsilon RNA(+) cells (r = 0.54, P =.02) and Cepsilon RNA(+) cells (r = 0.48, P =.05) when compared with the number of IL-4 mRNA(+) cells.
Increases in Iepsilon and Cepsilon RNA(+) cells, but not B-cell numbers, in the bronchial mucosa provide evidence for local IgE synthesis in both atopic and nonatopic asthma. These changes appear to relate to asthma rather than atopy per se and, at least in part, may be under the regulation of IL-4.
鼻黏膜中ε种系基因（Cε）转录本和ε重链基因（Iε）成熟mRNA的证实表明，过敏性鼻炎中可能发生IgE合成。
鉴于我们之前证实哮喘患者中IL-4 mRNA(+)细胞增加，我们评估了局部IgE合成是否也是支气管哮喘的一个特征。
从9名特应性哮喘患者和10名非特应性正常（内因性）对照受试者中获取纤维支气管镜黏膜活检标本。为了控制特应性，我们还研究了9名非特应性哮喘患者和10名特应性非哮喘对照受试者。对组织进行B细胞（CD20）免疫组织化学以及Iε和Cε RNA(+)细胞和IL-4 mRNA(+)细胞的原位杂交处理。
与对照受试者相比，哮喘患者支气管黏膜中的B细胞数量相似，而在特应性哮喘患者和非特应性哮喘患者中分别观察到显著更多的Iε RNA(+)细胞（分别为P = 0.02和P = 0.04）、Cε RNA(+)细胞（分别为P = 0.01和P = 0.03）和IL-4 mRNA(+)细胞（分别为P = 0.001和P = 0.001），但与非特应性对照受试者相比，特应性对照受试者中未观察到。在哮喘患者中，与IL-4 mRNA(+)细胞数量相比，Iε RNA(+)细胞（r = 0.54，P = 0.02）和Cε RNA(+)细胞（r = 0.48，P = 0.05）之间存在显著相关性。
支气管黏膜中Iε和Cε RNA(+)细胞增加，但B细胞数量未增加，这为特应性和非特应性哮喘中的局部IgE合成提供了证据。这些变化似乎与哮喘本身而非特应性有关，并且至少部分可能受IL-4调节。
