Zeibecoglou K, Ying S, Meng Q, Poulter L W, Robinson D S, Kay A B
Allergy and Clinical Immunology, Imperial College School of Medicine at the National Heart and Lung Institute, London, UK.
J Allergy Clin Immunol. 2000 Oct;106(4):697-704. doi: 10.1067/mai.2000.109824.
Previous studies have shown a prominent macrophage signal in the bronchial mucosa from nonatopic (intrinsic) compared with atopic (extrinsic) asthmatic subjects. This observation might have represented an expansion of a proinflammatory macrophage population or a homeostatic mechanism to decrease T(H)2-type inflammation.
The aim of the study was to investigate the numbers of macrophages and macrophage subpopulations and the expression of IL-10 and IL-12 in sputum from asthmatic and control subjects.
Eight atopic asthmatic (AA) subjects, 10 nonatopic asthmatic (NAA) subjects, 6 atopic control (AC) subjects, and 7 normal control (NC) subjects underwent sputum induction. Macrophages were enumerated by using Romanowsky stain and immunocytochemistry (CD68). RFD1 (interdigitating cell marker) and RFD7 (mature phagocyte marker) mAbs were used for immunocytochemical phenotyping, whereas IL-10 and IL-12 messenger (m)RNA was examined with in situ hybridization by using (35)S-labeled riboprobes. The phenotype of cells expressing IL-10 or IL-12 mRNA was examined by simultaneous in situ hybridization and immunostaining.
No differences in the numbers of CD68(+) macrophages and RFD1(+), RFD7(+), and RFD1(+)/RFD7(+) subpopulations were found between AA, NAA, AC, and NC subjects. However, the numbers of IL-10 and IL-12 mRNA(+) cells were increased in AA subjects compared with NAA, AC, and NC subjects (P <.05). No other differences were found among the groups. Most of the IL-10 and IL-12 mRNA(+) cells in sputum from asthmatic subjects were macrophages (>80%), with less than 10% of mRNA colocalizing to epithelial cells.
Sputum macrophage numbers, unlike tissue macrophages, as previously reported, were not elevated in NAA subjects. Increased IL-10 and IL-12 expression in atopic asthma may indicate the existence of a homeostatic mechanism to decrease lung inflammation. The lack of such cytokines in intrinsic asthma may predispose to bronchial inflammation in these subjects.
既往研究显示，与特应性（外源性）哮喘患者相比，非特应性（内源性）哮喘患者支气管黏膜中的巨噬细胞信号更为显著。这一观察结果可能代表促炎巨噬细胞群体的扩增或一种减轻T(H)2型炎症的稳态机制。
本研究旨在调查哮喘患者和对照者痰液中巨噬细胞及其亚群的数量以及白细胞介素-10（IL-10）和白细胞介素-12（IL-12）的表达情况。
8名特应性哮喘（AA）患者、10名非特应性哮喘（NAA）患者、6名特应性对照（AC）者和7名正常对照（NC）者接受痰液诱导。使用罗曼诺夫斯基染色和免疫细胞化学（CD68）对巨噬细胞进行计数。RFD1（交错突细胞标志物）和RFD7（成熟吞噬细胞标志物）单克隆抗体用于免疫细胞化学表型分析，而IL-10和IL-12信使核糖核酸（mRNA）则通过使用（35）S标记的核糖探针进行原位杂交检测。通过同时进行原位杂交和免疫染色来检查表达IL-10或IL-12 mRNA的细胞的表型。
在AA、NAA、AC和NC受试者之间，CD68(+)巨噬细胞以及RFD1(+)、RFD7(+)和RFD1(+)/RFD7(+)亚群的数量没有差异。然而，与NAA、AC和NC受试者相比，AA受试者中IL-10和IL-12 mRNA(+)细胞的数量增加（P <.05）。各亚组之间未发现其他差异。哮喘患者痰液中大多数IL-10和IL-12 mRNA(+)细胞是巨噬细胞（>80%），mRNA与上皮细胞共定位的比例不到10%。
与先前报道的组织巨噬细胞不同，NAA受试者痰液中的巨噬细胞数量并未升高。特应性哮喘中IL-10和IL-12表达增加可能表明存在一种减轻肺部炎症的稳态机制。内源性哮喘中缺乏此类细胞因子可能使这些受试者易患支气管炎症。
