Herz U, Braun A, Rückert R, Renz H
Department of Clinical Chemistry and Biochemistry, Virchow-Klinikum of the Humboldt-University Berlin, Germany.
Clin Exp Allergy. 1998 May;28(5):625-34. doi: 10.1046/j.1365-2222.1998.00280.x.
Bronchial asthma is characterized by a TH2 type immune response, chronic inflammation of the airways and increased airway responsiveness. The relationship between IgE- and inflammatory-dependent mechanisms that contribute to bronchial asthma are not well defined.
The purpose of this study was to compare and analyse the immune pathways that resulted in development of allergen-induced and/or inflammatory dependent increased airways responsiveness.
BALB/c and C57BL/6 mice responded to OVA-sensitization with elevated allergen-specific IgE/IgG1 serum antibody-titres and the development of cutaneous immediate-type hypersensitivity reactions. Increased airway responsiveness was observed following airway allergen challenges. However, the inflammatory component of the lung differed between the strains. In OVA-sensitized BALB/c mice a marked increase in lymphocytes, eosinophils and neutrophils in BAL fluids was parallelled with elevated production of IL-4, IL-5 and TNFalpha in the lung. In contrast in OVA-sensitized C57BL/6 mice, the inflammatory immune response in the lung was much weaker. We postulate that two pathways can regulate the induction of increased airway responsiveness. One depends on the presence of allergen-specific IgE/IgG1 and allergen, and a second is mediated by allergen-independent inflammation of the lung. To test this hypothesis, BALB/c mice were treated nasally with low doses of bacterial superantigen (SEB) as a prototypical inducer of airway inflammation, following which influx of lymphocytes, eosinophils and neutrophils into the airways was parallelled by development of increased airway-responsiveness in the absence of allergen-specific IgE/IgG1 antibodies and allergen.
These results indicate that increased airway responsiveness is associated with different immunological phenotypes in BALB/c and C57BL/6 mice.
支气管哮喘的特征为TH2型免疫反应、气道慢性炎症和气道反应性增加。导致支气管哮喘的IgE依赖性和炎症依赖性机制之间的关系尚未明确。
本研究的目的是比较和分析导致变应原诱导的和/或炎症依赖性气道反应性增加的免疫途径。
BALB/c和C57BL/6小鼠对卵清蛋白致敏的反应是变应原特异性IgE/IgG1血清抗体滴度升高以及皮肤速发型超敏反应的发生。气道变应原激发后观察到气道反应性增加。然而，两品系小鼠肺内的炎症成分有所不同。在卵清蛋白致敏的BALB/c小鼠中，支气管肺泡灌洗（BAL）液中淋巴细胞、嗜酸性粒细胞和中性粒细胞显著增加，同时肺内IL-4、IL-5和TNFα的产生也增加。相比之下，在卵清蛋白致敏的C57BL/6小鼠中，肺内的炎症免疫反应要弱得多。我们推测有两条途径可调节气道反应性增加的诱导。一条途径依赖于变应原特异性IgE/IgG1和变应原的存在，另一条途径由肺的变应原非依赖性炎症介导。为验证这一假设，给BALB/c小鼠经鼻给予低剂量细菌超抗原（SEB）作为气道炎症的典型诱导剂，随后淋巴细胞、嗜酸性粒细胞和中性粒细胞流入气道，同时在没有变应原特异性IgE/IgG1抗体和变应原的情况下气道反应性增加。
这些结果表明，BALB/c和C57BL/6小鼠气道反应性增加与不同的免疫表型有关。
