益生菌免疫调节功能研究

Effects on immunomodulatory of probiotics

目的:使用小鼠巨噬细胞和致敏模型小鼠探讨乳酸杆菌及双歧杆菌的菌株特异性免疫调节及抗过敏作用的可能性。方法:使用Lactobacillus acidophilus 6091(6091)、L.plantarum R-1-1(R-1-1)与小鼠巨噬细胞样细胞系J774A.1细胞(J774A.1细胞)进行共培养,用酶联免疫吸附测定法(enzyme-linked immunosorbent assay,ELISA)测定共培养上清液白细胞介素-6,10(Interleukin-6,10,IL-6,10)。使用R-1-1、6091、Bifidobacterium bifidum TMC3115(TMC3115)菌体对受试小鼠进行连续灌胃持续5周,在7、21、28 d分别注射卵清白蛋白(OVA)和氢氧化铝诱导其产生过敏反应,采用ELISA试剂盒检测血液总Ig E,同时用实时荧光定量PCR法检测脾脏细胞的IL-6、IL-12、TNF-α关于m RNA的表达。结果:各受试菌株有意地诱导J774A.1细胞产生IL-10、IL-6(P<0.05)。各受试菌株灌胃小鼠血液Ig E与OVA阳性对照组比较显著地降低(P<0.05);同时,各受试菌株灌胃小鼠脾脏细胞的IL-6、IL-12、TNF-α和OVA阳性对照组比较显著地降低(P<0.05);结论:6091、R-1-1、TMC3115能有效地通过活化巨噬细胞调节机体的免疫调节作用,降低血液Ig E产生,其作用机制可能与诱导IL-10的分泌,进而同时下调了TH1和TH2免疫应答有关。

This study aims to test the possibilities of Lactobacilli and Bifidobacteria against allergy by regulating the immunity of the host animal. Methods： Murine macrophage-like cell line J774 A.1 were co-cultured with the cells of Lactobacillus acidophilus 6091（6091）, L. plantarum R-1-1（R-1-1）. The supernatant of the J774 A.1 cell culture were collected for detecting production of interleukin-6（IL-6） and IL-10 using ELISA. The male BALB/C mice were orally administrated with the active cells of 6091, R-1-1 and Bifidobacterium bifidum TMC3115（TMC3115） for 5 weeks and were sensitized with ovalbumin（OVA） at day 7, 21 and 28. The serum total Ig E of the tested mice was analyzed with ELISA before and after the intervention. The expression of spleen IL-6, IL-12 and TNF-α m RNA in the tested mice were also evaluated with Quantitative Real-time PCR. Results： Each of tested bacteria significantly stimulated J774 A. 1 cells to produce IL-6 and IL-10 in a strain dependent manner（P〈0.05）. The increased of serum Ig E of the tested mice were also decreased significantly by the treatment of three bacteria（P〈0.05）. The expression of the spleen IL-6, IL-12, TNF-α m RNA of the tested mice was also significantly suppressed by the orally fed bacteria（P〈0.05）. Conclusion： These results indicated that lactobacilli and bifidobacteria could inhibit Ig E mediated allergic disorder by suppressing the serum Ig E production caused by food allergens. One of the possible underlying mechanism might be the abilities of these bacteria to stimulate IL-10 production by which to down-regulate the hyper-immune responses including both Th1 and Th2 types.