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Modification of the animal immune system by feeding probiotics

机译:通过喂养益生菌来改变动物的免疫系统

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摘要

The objective of this study was to examine immune effects of feeding novel probiotic Lactobacillus acidophilus strain NP51 to specific pathogen-free Balb/c mice challenged with Mycobacterium avium subspecies paratuberculosis (MAP), the causative agent of Johne\u27sdisease (JD). We hypothesized that feeding the NP51 would activate the adaptive immunity and impede the development of MAP infection in murine model of JD. Thus, Balb/c mice were randomized to treatment groups in a factorial design including mice that either fed the heat-killed or viable NP51 (HNP51 or VNP51, respectively) and challenged with either a heat-killed or a viable MAP (HMAP or VMAP, respectively). Mice were fed 1 × 106 CFU of either HNP51 orVNP51*mice-1*day-1 mixed with standard mouse chow until the end of the study. Subsequently, mice were challenged with 1 × 108 CFU of HMAP or VMAP injected intraperitonealy on day 45 of the study. Ten mice from each group were euthanized on days 45, 90, 135, and 180. Spleens were excised and used for an in vitro splenocytes cell cultures that were either stimulated with sonicated MAP antigen or concanavalin A and examined for the cytokine secretion pattern andfrequency of T lymphocyte subpopulations. Blood was withdrawn by cardiac puncture and used for examination of immunoglobulins production. HNP51 and VNP51 differentially stimulated the adaptive immunity and decrease MAP tissue burden. With VMAP as the inoculum, both VNP51 and HNP51 stimulated CD8α+ immune cell-mediated immunity and decreased the humoral immunity. When HMAP was used as the inoculum, VNP51 stimulated the CD8α+ immune cells-mediated and the humoral immunity. In contrast, HNP51 feeding induced CD8α+ immune cells-mediated immunity only as verified by the differential cytokines and immunoglobulins secretion pattern. The data provide persuasive evidence that NP51 has the potency to prevent JD infection in murine model of JD.
机译:这项研究的目的是研究将新型益生菌嗜酸乳杆菌菌株NP51喂入特定无病原体的Balb / c小鼠的免疫效果,这些小鼠受到鸟分枝杆菌亚种副结核病(MAP)的攻击,而后者是约翰内氏病(JD)的病原体。我们假设饲喂NP51会激活JD鼠模型的适应性免疫并阻碍MAP感染的发展。因此,将Balb / c小鼠按因子设计随机分配至治疗组,包括喂食热杀死或存活的NP51(分别为HNP51或VNP51)并接受热杀死或存活的MAP(HMAP或VMAP)攻击的小鼠, 分别)。给小鼠喂食1×106 CFU的HNP51或VNP51 *小鼠-1 * day-1与标准小鼠食物混合,直至研究结束。随后,在研究的第45天,用腹膜内注射的1×108 CFU HMAP或VMAP攻击小鼠。在第45、90、135和180天对每组十只小鼠实施安乐死。切除脾脏,用于体外脾细胞培养,用超声处理的MAP抗原或伴刀豆球蛋白A刺激,检查细胞因子的分泌模式和频率。 T淋巴细胞亚群。通过心脏穿刺抽血,用于检查免疫球蛋白的产生。 HNP51和VNP51差异性地刺激了适应性免疫并降低了MAP组织的负担。以VMAP为接种体,VNP51和HNP51均可刺激CD8α+免疫细胞介导的免疫,并降低体液免疫。当HMAP用作接种物时,VNP51刺激CD8α+免疫细胞介导的和体液免疫。相比之下,HNP51喂养仅诱导了CD8α+免疫细胞介导的免疫,这已通过不同的细胞因子和免疫球蛋白的分泌方式得到证实。数据提供了有说服力的证据,表明NP51在JD鼠模型中具有预防JD感染的能力。

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  • 作者

    Osman, Mohamed Abdulraheem;

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  • 年度 2011
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  • 原文格式 PDF
  • 正文语种 en
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