Maeda Y, Musoh K, Shichijo M, Tanaka H, Nagai H
Department of Pharmacology, Gifu Pharmaceutical University, Japan.
Pharmacology. 1997 Jul;55(1):32-43. doi: 10.1159/000139510.
The effects of IFN-beta and prednisolone (Pred) on antigen-induced IgE antibody production, airway eosinophilia and airway hyperreactivity (AHR) were studied in ovalbumin-sensitized Balb/c mice. Three inhalations of antigen (ovalbumin) caused an increase in the number of eosinophils and lymphocytes in bronchoalveolar lavage fluid and AHR to acetylcholine with a significant elevation in the serum IgE level. IFN-beta clearly inhibited the antigen-induced airway inflammation and AHR, but did not affect IgE antibody production. Pred inhibited antigen-induced IgE antibody production, airway inflammation and AHR to acetylcholine. In addition, IFN-beta inhibited T-helper type 2 (Th2) cell clone (D10G4.1)-induced peritoneal eosinophilia in mice, but did not affect neutrophilia, whereas Pred inhibited D10G4.1-induced peritoneal eosinophilia and neutrophilia. These results suggest that IFN-beta inhibits antigen-induced bronchial inflammation and AHR probably due to the inhibition of Th2-induced airway eosinophilia.
在卵清蛋白致敏的Balb/c小鼠中研究了干扰素-β（IFN-β）和泼尼松龙（Pred）对抗原诱导的IgE抗体产生、气道嗜酸性粒细胞增多和气道高反应性（AHR）的影响。三次吸入抗原（卵清蛋白）导致支气管肺泡灌洗液中嗜酸性粒细胞和淋巴细胞数量增加，对乙酰胆碱的气道高反应性增强，血清IgE水平显著升高。IFN-β明显抑制抗原诱导的气道炎症和气道高反应性，但不影响IgE抗体产生。Pred抑制抗原诱导的IgE抗体产生、气道炎症和对乙酰胆碱的气道高反应性。此外，IFN-β抑制小鼠中2型辅助性T细胞（Th2）克隆（D10G4.1）诱导的腹膜嗜酸性粒细胞增多，但不影响中性粒细胞增多，而Pred抑制D10G4.1诱导的腹膜嗜酸性粒细胞增多和中性粒细胞增多。这些结果表明，IFN-β抑制抗原诱导的支气管炎症和气道高反应性可能是由于抑制了Th2诱导的气道嗜酸性粒细胞增多。
