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IFN-γ对小鼠急性过敏性气道炎症的抑制作用 被引量:2

IFN-γ inhibits acute allergic airway inflammation in mice
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摘要 目的 探究IFN-γ对IL-33诱导的小鼠急性过敏性气道炎症中2型固有淋巴细胞(ILC2s)的抑制作用.方法 将24只6~8周的雌性C57BL/6小鼠随机分为4组:IL-33模型组、单独IFN-γ组、IL-33+IFN-γ联合刺激组、PBS对照组.用IL-33成功构建小鼠支气管过敏性炎症模型,收集支气管肺泡灌洗液(BALF)和肺组织,使用流式细胞术对ILC2s和嗜酸性粒细胞进行分析.酶联免疫吸附法(ELISA)测定肺匀浆和BALF上清中IL-5和IL-13的含量.Real-time PCR检测IL-5、IL-13和ST2 mRNA表达量的变化.肺组织切片进行HE和PAS染色观察病理变化.结果 与PBS对照组相比,IFN-γ组未见炎细胞浸润、杯状细胞增生及黏液分泌;ILC2s和嗜酸性粒细胞含量无差异(P〉0.05);IL-5、IL-13水平差异无统计学意义(P〉0.05);IL-5、IL-13、ST2 mRNA表达量差异无统计学意义(P〉0.05).与PBS对照组相比,IL-33模型组有大量炎性细胞浸润,杯状细胞增生并分泌大量黏液;ILC2s和嗜酸性粒细胞含量明显增多,差异有统计学意义(P〈0.05);IL-5、IL-13水平升高,差异有统计学意义(P〈0.05);IL-5、IL-13、ST2 mRNA表达量增高,差异有统计学意义(P〈0.05).与IL-33组相比,IFN-γ+IL-33组炎细胞浸润减弱,杯状细胞增生受到抑制且黏液分泌量减少;IL-5、IL-13水平降低,差异有统计学意义(P〈0.05);IL-5、IL-13、ST2 mRNA表达量降低,差异有统计学意义(P〈0.05).结论 实验证实IFN-γ可抑制IL-33引起的嗜酸性粒细胞和ILC2s的增殖,减弱IL-5、IL-13的分泌,提示:IFN-γ对IL-33诱导的小鼠急性过敏性气道炎症有抑制作用. Objective To investigate the inhibitory effect of IFN-γ on acute allergic airway inflammation induced by IL-33 in mice.Methods Twenty-four female C57BL/6 mice (6-8 weeks) were randomly divided into four groups: IL-33 model group, IFN-γ treatment group, IL-33+IFN-γ treatment group and PBS control group.A mouse model of acute allergic airway inflammation was induced by IL-33.Samples of bronchial alveolar lavage fluid (BALF) and lung tissues were collected.Group 2 innate lymphoid cells (ILC2s) and eosinophils were analyzed by flow cytometry.Levels of IL-5 and IL-13 in the supernatants of lung homogenate and BALF were measured by ELISA.Expression of IL-5, IL-13 and ST2 at mRNA level was detected by real-time PCR.Pathological changes in lung tissues were observed following hematoxylin and eosin (HE) and periodic acid-Schiff (PAS) staining.Results Compared with the PBS control group, no infiltration with inflammatory cells, goblet cell hyperplasia or mucus secretion was observed in the IFN-γ group;the numbers of ILC2s and eosinophils were not affected by IFN-γ;the levels of IL-5 and IL-13 in the supernatants of BALF and lung homogenate, and the expression of IL-5, IL-13 and ST2 at mRNA level in lung tissues were not significantly changed by IFN-γ (P〉0.05).Compared with the PBS control group, massive infiltration with inflammatory cells, excessive mucus secretion, increased numbers of ILC2s and eosinophils, up-regulated levels of IL-5 and IL-13 in the supernatants of BALF and lung homogenate, and enhanced expression of IL-5, IL-13 and ST2 at mRNA level in lung tissues were detected in the IL-33 model group (P〈0.05).Compared with the IL-33 model group, the combined treatment with IL-33 and IFN-γ significantly alleviated inflammatory cell infiltration, inhibited mucus secretion, reduced the numbers of ILC2s and eosinophils, down-regulated the levels of IL-5 and IL-13 in the supernatants of BALF and lung homogenate, and suppressed the expression of IL-5, IL-13 and ST2 at mRNA in l
出处 《中华微生物学和免疫学杂志》 CAS CSCD 北大核心 2017年第8期573-579,共7页 Chinese Journal of Microbiology and Immunology
关键词 干扰素-Γ 2型固有淋巴细胞 白细胞介素-33 过敏性气道炎症 IFN-γ Group 2 innate lymphoid cell IL-33 Acute airway inflammation
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