CAJ | 학술논문

目的研究青春型双歧杆菌对过敏性哮喘儿童外周血单个核细胞来源的树突状细胞(dendritic cells,DC)表面共刺激分子表达及其细胞因子分泌的影响.方法从15例过敏性哮喘儿童和15例非哮喘儿童的外周血单个核细胞诱导生成未成熟DC,与青春型双歧杆菌共培养48小时后,用流式细胞仪检测DC表面CD86和HLA-DR分子的表达,用ELISA方法检测培养上清中自细胞介素(IL)-10、IL-12和IFN-γ的水平.结果经双歧杆菌刺激后,哮喘儿童DC表面CD86表达明显增高(P<0.05),DC分泌IL-12和IFN-γ水平明显增高;而双歧杆菌刺激对非哮喘儿童的CD86和HLA-DR表达无明显影响,但可使其DC分泌IL-12及IL-10水平明显增高.结论青春型双歧杆菌既可以通过上调CD86的表达,促进DC成熟;又可刺激DC分泌IL-12和IFN-γ,改变Th2优势分化,纠正TH1/Th2失衡,这可能是益生菌防治变态反应性疾病的机制之一.
목적 연구청춘형쌍기간균대과민성효천인동외주혈단개핵세포래원적수돌상세포(dendritic cells,DC)표면공자격분자표체급기세포인자분비적영향.방법 종15례과민성효천인동화15례비효천인동적외주혈단개핵세포유도생성미성숙DC,여청춘형쌍기간균공배양48소시후,용류식세포의검측DC표면CD86화HLA-DR분자적표체,용ELISA방법검측배양상청중자세포개소(IL)-10、IL-12화IFN-γ적수평.결과 경쌍기간균자격후,효천인동DC표면CD86표체명현증고(P<0.05),DC분비IL-12화IFN-γ수평명현증고;이쌍기간균자격대비효천인동적CD86화HLA-DR표체무명현영향,단가사기DC분비IL-12급IL-10수평명현증고.결론 청춘형쌍기간균기가이통과상조CD86적표체,촉진DC성숙;우가자격DC분비IL-12화IFN-γ,개변Th2우세분화,규정TH1/Th2실형,저가능시익생균방치변태반응성질병적궤제지일.
Objective To evaluate the effects of Bifidobacterium adolescent on the function of dendritic cells(DC) derived from peripheral blood mononuclear cells (PBMC) of the children with allergic asthma. Methods The PBMC-derived DC were proliferated in the presence of granulocyte macrophage-colony stimulating factor (GM-CSF) and interleukin-4 (IL-4) from 15 patients with allergic asthma and 15 normal children, and then the immature DC were cocultured with the Bifidobacterium adolescent for 48 h. The expression of CD86 and HLA-DR of DC were measured by flow cytometer. The IL-10, IL-12, and IFN-γ levels of culture supernatant were measured by ELISA. Results After the preprocessing with Bifidobacterium adolescent, the expression of CD86 on the DC, and secretion IL-12 and IFN-γ from the patients with allergic asthma were significantly increased (P < 0.05). The preprocessing with the Bifidobacterium adolescent has no effects on the expression of CD86 and HLA-DR on the DC of the control group, but could increased the level of IL-12 and IL-10 significantly. Conclusions The Bifidobacterium adolescent can not only stimulate the maturation of DC from the patients with allergic asthma by up-regulating the expression of CD86, but also stimulate the DC to secret the IL-12 and IFN-γ. It may alter Th2 dominant differentiation and retrieve the Th1/Th2 imbalance in allergic asthma. t