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烟曲霉抗原诱导的小鼠嗜酸性粒细胞增多症可被抗白细胞介素-5抗体消除。

Aspergillus fumigatus antigen induced eosinophilia in mice is abrogated by anti-IL-5 antibody.

作者信息

Murali P S, Kumar A, Choi H, Banasal N K, Fink J N, Kurup V P

机构信息

Allergy and Immunology Division, Medical College of Wisconsin, Milwaukee.

出版信息

J Leukoc Biol. 1993 Mar;53(3):264-7. doi: 10.1002/jlb.53.3.264.

DOI:10.1002/jlb.53.3.264
PMID:8454950
Abstract

A murine model of allergic bronchopulmonary aspergillosis (ABPA), developed by exposure to Aspergillus fumigatus antigens, demonstrated eosinophilia of peripheral blood (PB), bone marrow (BM), and lung. The eosinophilia was abrogated by monoclonal anti-interleukin-5 (IL-5) antibody (TRFK-5) and not by an isotype control antibody (GL 113). Eosinophils in PB were enumerated from stained smears and their relative increase or decrease in cells from BM and lung was determined by an eosinophil peroxidase (EPO) assay (measured in optical density). Intraperitoneal injection of TRFK-5 in mice exposed to A. fumigatus antigen produced a significant reduction in eosinophils (PB 6.6 +/- 1.14% vs. 3.8 +/- 0.8%, P < .01) and EPO production in BM (0.935 +/- 0.03 vs. 0.615 +/- 0.02, P < .001). A similar reduction in EPO production in the lung (0.691 +/- 0.12 vs. 0.495 +/- 0.05, not significant) was also reflected in the histopathology for the different groups of mice. These findings confirming the role of IL-5 in eosinophilia, although not surprising, are significant in elucidating the immunopathogenesis of ABPA in the murine model. We conclude that in this model, eosinophilia may be due largely to the Th2 cytokine -IL-5 induced by A. fumigatus antigens.

摘要

通过暴露于烟曲霉抗原建立的变应性支气管肺曲霉病(ABPA)小鼠模型,表现出外周血(PB)、骨髓(BM)和肺的嗜酸性粒细胞增多。嗜酸性粒细胞增多可被抗白细胞介素-5(IL-5)单克隆抗体(TRFK-5)消除,而异型对照抗体(GL 113)则无此作用。从染色涂片上计数PB中的嗜酸性粒细胞,并通过嗜酸性粒细胞过氧化物酶(EPO)测定法(以光密度测量)确定BM和肺中细胞的相对增减。对暴露于烟曲霉抗原的小鼠腹腔注射TRFK-5,可使嗜酸性粒细胞显著减少(PB:6.6±1.14%对3.8±0.8%,P<.01),并使BM中的EPO产生减少(0.935±0.03对0.615±0.02,P<.001)。肺中EPO产生的类似减少(0.691±0.12对0.495±0.05,无显著性差异)也反映在不同组小鼠的组织病理学中。这些发现证实了IL-5在嗜酸性粒细胞增多中的作用,尽管并不令人惊讶,但对于阐明小鼠模型中ABPA的免疫发病机制具有重要意义。我们得出结论,在该模型中,嗜酸性粒细胞增多可能主要归因于烟曲霉抗原诱导的Th2细胞因子IL-5。

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