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乳酸菌对尘螨致哮喘小鼠的免疫调节及对P38通路的影响
引用本文:于宝丹,李理,徐军. 乳酸菌对尘螨致哮喘小鼠的免疫调节及对P38通路的影响[J]. 中国免疫学杂志, 2005, 21(9): 697-700
作者姓名:于宝丹  李理  徐军
作者单位:广州医学院,广州呼吸疾病研究所,广州,510120
基金项目:本课题受国家自然科学基金项目(30230180)、教育部科学技术研究重点项目(03099)、广东省自然科学基金项目(34649)资助.
摘    要:目的:比较乳酸乳球菌及植物乳杆菌对尘螨变应原致哮喘小鼠的免疫调节作用及对P38通路的影响。方法:将实验小鼠分生理盐水组、单纯尘螨致敏激发及尘螨致敏激发同时分别用乳酸乳球菌及植物乳杆菌灌胃组,进行肺泡灌洗并对肺泡灌洗液(BALF)细胞计数及嗜酸性粒细胞(EOS)计数,ELISA法检测经尘螨刺激的脾细胞72小时培养上清的IL-4水平,Western blot法检测脾细胞中P38总蛋白及磷酸化的P38水平。结果:哮喘组BALF细胞总数、EOS计数、脾细胞IL-4水平均比生理盐水组明显增高(P<0.05),乳酸乳球菌组较哮喘组上述指标显著减低(P<0.05),而植物乳杆菌组与哮喘组比则无明显差异(P>0.05)。哮喘组与植物乳杆菌组磷酸化P38表达水平较正常对照组显著增高,乳酸乳球菌组与对照组比较基本无变化。结论:乳酸乳球菌可改善尘螨所致的小鼠哮喘反应,其免疫调节可能与P38通路的抑制有关。

关 键 词:乳酸菌 哮喘 免疫调节 P38
文章编号:1000-484X(2005)09-0697-04
收稿时间:2004-03-12
修稿时间:2004-03-12

Effects of lactic acid bacteria on P38 signaling in immune response to dust mite in mite-sensitized mice
YU Bao-Dan,LI Li,XU Jun. Effects of lactic acid bacteria on P38 signaling in immune response to dust mite in mite-sensitized mice[J]. Chinese Journal of Immunology, 2005, 21(9): 697-700
Authors:YU Bao-Dan  LI Li  XU Jun
Abstract:Objective:To investigate the effect of lactic acid bacteria on P38 signaling in immune response to dust time in mite-sensitized mice.Methods:40 C57BL/6 mice in Group M,P and C,except for N(saline control),were sensitized and challenged with mite extract.Mice in C and P were simultaneously fed to Lactococcus lactis and Lactobacillus respectively.Total cell count and classification in BALF were done and IL-4 level detected by ELISA.Western blot were performed for detection of P38 signaling from mice's spleen cells stimulated with mite extract.Results:IL-4 level,total cell count and the percentage of eosinophils in BALF were significantly lower in Group C(P<0.05) than those in Group M(mite-sensitized mice without LAB treatment),but not in Group P.P38 signaling in spleen cells was activated in the mice of Group M,similarly in mice of Group P,but not of Group C.Conclusion:Oral treatment of Lactococcus lactis could to induce an immune tolerance in response to mite by inhibiting activation of P38 signaling.
Keywords:Lactic acid bacteria   Asthma   Immune regulation   P38
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