LPSp辅佐HBsAg诱导机体产生特异性抗体的机制  被引量:6

Mechanism of the effect of LPSp on the production of anti-HBs in mice

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作  者:王健[1] 冷静[2] 王启辉[2] 

机构地区:[1]广西医科大学第一附属医院临床医学实验中心,广西南宁530021 [2]广西医科大学基础医学院微生物学与免疫学教研室,广西南宁530021

出  处:《细胞与分子免疫学杂志》2007年第6期559-561,共3页Chinese Journal of Cellular and Molecular Immunology

基  金:广西医科大学博士基金项目(2004年)

摘  要:目的:研究革兰阴性非致病性成团泛菌脂多糖(LPSp)作为佐剂促进乙型肝炎表面抗原蛋白(HBsAg)诱导小鼠产生抗-HBs抗体的作用机制。方法:在体外用LPSp+HBsAg、HBsAg、LPSp、生理盐水分别致敏小鼠腹腔巨噬细胞,观察致敏细胞回输体内后诱导HBs抗体产生水平,检测巨噬细胞培养上清中TNF-α活性和NO浓度;观察4组巨噬细胞吞噬功能变化,并检测致敏巨噬细胞诱导局部淋巴结细胞分泌IL-4和IFN-γ的能力。结果:HBsAg+LPSp致敏巨噬细胞促进小鼠HBs抗体产生,LPSp致敏的巨噬细胞的吞噬能力显著增强(P<0.05),释放TNF-α和NO水平增加(P<0.05)。LPSp+HBsAg致敏巨噬细胞诱导局部淋巴结细胞释放IL-4水平升高(P<0.05),诱导IFN-γ水平与单纯HBsAg致敏组差异无统计学意义(P>0.05)。结论:LPSp的佐剂机制为参与活化巨噬细胞,增强巨噬细胞对抗原的吞噬、消化和处理能力;同时促进HBsAg致敏的巨噬细胞诱导淋巴结内淋巴细胞释放IL-4,增强HBsAg致敏的巨噬细胞诱导Th2淋巴细胞活化,促进B细胞产生抗体。AIM: To investigate the mechanism of the effect of avirulent Pantoea agglomerans lipopolysaccharide (LPSp) as the adjuvant of HBsAg on the production of anti- HBs in mice. METHODS: The peritoneal macrophages of BALB/c mice were pulsed in vitro by HBsAg + LPSp, HBsAg, LPSp, and NS respectively. The levels of anti-HBs IgG in serum were determined by ELISA. The variation of phagocytosis of the macrophages was detected. The culture supernatants were harvested and assayed for TNF-α and NO. HBsAg-pulsed peritoneal macrophages in the presence or absence of LPSp were injected in the hind footpads of syngeneic mice. Lymph node cells were harvested and cultured by HBsAg. IL-4 and IFN-γ in the supematants were quantitated by ELISA. RESULTS: The titer of anti-HBs IgG from the mice immunized with HBsAg-pulsed peritoneal macrophages treated with LPSp was higher than that of the mice immunized in the absence of LPSp. The phagocytosis rate of the LPSp-treated peritoneal macrophages was higher than that of the untreated macrophages. The level of TNF-α and NO of the LPSp-treated peritoneal macrophages was higher than that of the untreated macrophages. HBsAg- pulsed peritoneal cells in the presence of LPSp can induced higher production of IL-4 than those in the absence of LPSp. CONCLUSION: LPSp can act as the adjuvant of HBsAg and effectively increase the anti-HBS in the mice immunized by HBsAg. LPSp can activate macrophages and stimulate HBsAg-pulsed macrophages to induce the production of IL-4 of lymph node cells.

关 键 词:LPSP 乙型肝炎表面抗原 巨噬细胞 

分 类 号:R392.11[医药卫生—免疫学]

 

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