Nongenetically modified Lactococcus lactis-adjuvanted vaccination enhanced innate immunity against Helicobacter pylori.
Nongenetically modified Lactococcus lactis-adjuvanted vaccination enhanced innate immunity against Helicobacter pylori.
复制标题
非转基因乳酸乳球菌辅助疫苗接种增强了针对幽门螺杆菌的先天免疫力。
DOI：
10.1111/hel.12426
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发表时间：
2017
期刊：
影响因子：
4.4
通讯作者：
Xing Yingying
中科院分区：
文献类型：
--
作者：
Liu Wei;Tan Zhoulin;Liu Hai;Zeng Zhiqin;Luo Shuanghui;Yang Huimin;Zheng Lufeng;Xi Tao;Xing Yingying
乳酸乳球菌产生的革兰氏阳性增强基质颗粒（GEM）可以增强疫苗诱导的免疫应答。然而，这种佐剂增强口服疫苗效力的机制仍未得到探索。材料与方法采用小鼠预防模型研究GEM佐剂疫苗接种的机制。采用ELISA法检测小鼠血清中幽门螺杆菌特异性抗体反应。检测脲酶特异性脾细胞因子谱。在第43天和第71天，通过实时定量PCR、流式细胞术和组织学检测胃炎症反应。结果中药复方GEM对口腔健康有明显的促进作用。幽门螺杆菌疫苗通过促进先天免疫由GEM颗粒和重组抗原CTB‐UE组成的CUE‐GEM疫苗对免疫小鼠具有保护作用。pyloriinsult。保护性反应与刺激后胃炎的诱导和局部Th1/Th17细胞药物免疫反应有关。我们发现，先天炎症反应包括中性粒细胞趋化因子CXCL1‐2、中性粒细胞和抗菌蛋白S100A8和MUC1显著升高。在所有感染小鼠中，S100A8和MUC1水平与h呈负相关。pyloriburden。引人注目的是，接受GEM治疗的小鼠也显示出定植减少，这可能是通过自然宿主反应途径募集CD4+T细胞并促进S100A8表达。结论基于GEM的疫苗可能影响Th1/Th17免疫，从而协调对sth的先天免疫反应。pyloriinfection。
BackgroundGram‐positive enhancer matrix particles (GEM) produced byLactococcus lactiscan enhance vaccine‐induced immune response. However, the mechanism under which this adjuvant mounts the efficacy of orally administered vaccines remains unexplored.Materials and MethodsWe used a prophylactic mice model to investigate the mechanism of GEM‐adjuvanted vaccination.Helicobacter pyloriurease‐specific antibody response was monitored and detected in murine serum by ELISA. Urease‐specific splenic cytokine profile was examined. Gastric inflammatory responses were measured on day 43 or 71 by quantitative real‐time PCR, flow cytometry and histology.ResultsWe found that GEM enhanced the efficiency of oralH. pylorivaccine by promoting innate immunity. The vaccine CUE‐GEM composed of GEM particles and recombinant antigen CTB‐UE provided protection of immunized mice againstH. pyloriinsult. The protective response was associated with induction of postimmunization gastritis and local Th1/Th17 cell‐medicated immune response. We showed that innate inflammatory responses including neutrophil chemokines CXCL1‐2, neutrophils, and antimicrobial proteins S100A8 and MUC1 were significantly elevated. Within all infected mice, S100A8 and MUC1 levels were negatively correlated withH. pyloriburden. Strikingly, mice receiving GEM also show reduction of colonization, possibly through natural host response pathways to recruit CD4+T cells and promote S100A8 expression.ConclusionsThese findings suggest that GEM‐based vaccine may impact Th1/Th17 immunity to orchestrate innate immune response againstH. pyloriinfection.