Virchow J C, Kroegel C, Walker C, Matthys H
Department of Pneumology, University Medical Clinic, Freiburg, Germany.
J Allergy Clin Immunol. 1996 Nov;98(5 Pt 2):S27-33; discussion S33-40.
Cellular and mediator profiles in bronchoalveolar lavage have not been compared systematically between patients with asthma of different severities, mainly because the patients with more severe asthma have an increased need for antiinflammatory medication. Information is limited to comparisons of allergic and intrinsic asthma, which can be distinguished clinically. When patients from these two groups with similar degrees of bronchial hyperresponsiveness were compared, both groups showed increased numbers of activated T-helper lymphocytes; those in the allergic group expressed the IL-2 receptor (CD25+), whereas in patients with intrinsic asthma there was also an increased number of T-suppressor cells with the activation markers CD25, class II histocompatibility antigen, and very late activation antigen-I, as well as T-helper cells class II histocompatibility antigen and very late activation antigen-I. This pattern is compatible with a more chronic T-cell activation in patients with intrinsic asthma. In patients with allergic asthma the cytokine pattern is compatible with a pure TH2 response (elevated IL-4 and IL-5); however, intrinsic asthma is characterized by elevated IL-5 and IL-2 but not IL-4. Our own findings show similar concentrations of IL-1, IL-8, and granulocyte-macrophage colony-stimulating factor in bronchoalveolar lavage fluid of patients with allergic and intrinsic asthma, whereas IL-6 and interferon-gamma tended to be higher in patients with intrinsic asthma. There are probably fundamental differences in the pathogenesis of allergic and intrinsic asthma. These findings suggest that asthma does not depend on the presence of IgE or IL-4, although both may contribute to the pathogenesis of atopic asthma. The only common pathway in the different presentations of asthma that has been related to clinical symptoms appears to be IL-5-mediated activation of eosinophils; therapies aimed at this mechanism may be promising.
不同严重程度哮喘患者的支气管肺泡灌洗中的细胞和介质特征尚未得到系统比较，主要原因是重度哮喘患者对抗炎药物的需求增加。相关信息仅限于对过敏性哮喘和内源性哮喘的比较，这两种哮喘在临床上可以区分。当比较这两组支气管高反应性程度相似的患者时，两组活化的辅助性T淋巴细胞数量均增加；过敏性哮喘组的细胞表达白细胞介素-2受体（CD25+），而内源性哮喘患者中具有CD25、Ⅱ类组织相容性抗原和极晚期活化抗原-I等活化标志物的抑制性T细胞数量也增加，同时辅助性T细胞的Ⅱ类组织相容性抗原和极晚期活化抗原-I也增加。这种模式与内源性哮喘患者更慢性的T细胞活化相一致。在过敏性哮喘患者中，细胞因子模式与单纯的TH2反应（白细胞介素-4和白细胞介素-5升高）相一致；然而，内源性哮喘的特征是白细胞介素-5和白细胞介素-2升高，但白细胞介素-4不升高。我们自己的研究结果显示，过敏性哮喘和内源性哮喘患者的支气管肺泡灌洗液中白细胞介素-1、白细胞介素-8和粒细胞-巨噬细胞集落刺激因子浓度相似，而内源性哮喘患者的白细胞介素-6和干扰素-γ往往更高。过敏性哮喘和内源性哮喘的发病机制可能存在根本差异。这些发现表明，哮喘并不依赖于免疫球蛋白E或白细胞介素-4的存在，尽管两者可能都参与特应性哮喘的发病机制。在与临床症状相关的哮喘不同表现形式中，唯一的共同途径似乎是白细胞介素-5介导的嗜酸性粒细胞活化；针对这一机制的治疗可能很有前景。
