Brown J L, Behndig A F, Sekerel B E, Pourazar J, Blomberg A, Kelly F J, Sandström T, Frew A J, Wilson S J
Allergy and Inflammation Research, University of Southampton, Southampton, UK.
Clin Exp Allergy. 2007 May;37(5):688-95. doi: 10.1111/j.1365-2222.2007.02695.x.
BACKGROUND: Allergic rhinitis (AR) and asthma represent a continuum of atopic disease. AR is believed to pre-dispose an individual to asthma. Compared with asthmatics and normal controls, the inflammatory response in the lower airways of rhinitics is not fully elucidated. To test the hypothesis that the inflammatory response in the airways of subjects with AR is at a level intermediate between that in normal controls and asthmatics, we have characterized bronchial inflammation and cytokine mRNA levels in non-asthmatic allergic rhinitics and compared it with subjects with allergic asthma and with normal controls. METHODS: Endobronchial mucosal biopsies were obtained at bronchoscopy from 14 allergic rhinitics, 16 asthmatics and 21 normal controls. Biopsies were embedded into glycol methacrylate resin for immunohistochemical analysis of cellular inflammation and snap frozen for semi-quantitative PCR analysis of cytokine mRNA levels. RESULTS: Airway inflammation in rhinitic subjects was characterized by an increase in submucosal eosinophils, mast cells and the mRNA expression of TNF-alpha, at an intermediate level between healthy and asthmatics. In addition, CD3(+) and CD8(+) lymphocytes in the epithelium, the endothelial expression of vascular adhesion molecule-1 and IL-1 beta mRNA were higher in the allergic rhinitics compared with both normal controls and asthmatics, whereas growth-related oncogene alpha-mRNA was decreased in AR compared with both healthy and asthmatics. Airway inflammation in the asthmatic group was characterized by higher numbers of eosinophils and mast cells, together with an increase in TNF-alpha-mRNA compared with both healthy and rhinitics. IFN-gamma mRNA was the highest in normal controls and lowest in the asthmatics. CONCLUSIONS: In individuals with AR the present data suggest an intermediate state of airway inflammation between that observed in normal individuals and subjects with clinical asthma. It is also indicated that IFN-gamma production by CD8(+) T lymphocytes could be protective against the development of airway hyperresponsiveness. Further work is needed to evaluate this hypothesis.
背景：变应性鼻炎（AR）和哮喘是特应性疾病的连续谱。AR被认为会使个体易患哮喘。与哮喘患者和正常对照相比，鼻炎患者下呼吸道的炎症反应尚未完全阐明。为了验证AR患者气道炎症反应水平介于正常对照和哮喘患者之间这一假设，我们对非哮喘性变应性鼻炎患者的支气管炎症和细胞因子mRNA水平进行了特征分析，并将其与变应性哮喘患者和正常对照进行比较。 方法：在支气管镜检查时从14例变应性鼻炎患者、16例哮喘患者和21例正常对照获取支气管黏膜活检标本。将活检标本包埋于甲基丙烯酸乙二醇酯树脂中用于细胞炎症的免疫组织化学分析，并速冻用于细胞因子mRNA水平的半定量PCR分析。 结果：鼻炎患者的气道炎症特征为黏膜下嗜酸性粒细胞、肥大细胞增多以及肿瘤坏死因子-α（TNF-α）mRNA表达增加，处于健康人和哮喘患者之间的中间水平。此外，与正常对照和哮喘患者相比，变应性鼻炎患者上皮中的CD3(+)和CD8(+)淋巴细胞、血管黏附分子-1的内皮表达以及白细胞介素-1β（IL-1β）mRNA更高，而与健康人和哮喘患者相比，变应性鼻炎患者中生长相关癌基因α（GRO-α）mRNA降低。哮喘组的气道炎症特征为嗜酸性粒细胞和肥大细胞数量更多，与健康人和鼻炎患者相比，TNF-α mRNA也增加。γ干扰素（IFN-γ）mRNA在正常对照中最高，在哮喘患者中最低。 结论：目前的数据表明，AR患者的气道炎症处于正常个体和临床哮喘患者之间的中间状态。还表明CD8(+) T淋巴细胞产生的IFN-γ可能对气道高反应性的发展具有保护作用。需要进一步开展工作来评估这一假设。
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