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Bifidobacterium thermophilum RBL67 impacts on growth and virulence gene expression of Salmonella enterica subsp enterica serovar Typhimurium

机译:嗜热双歧杆菌RBL67对肠炎沙门氏菌肠型血清鼠伤寒沙门氏菌的生长和毒力基因表达的影响

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摘要

Background: Bifidobacterium thermophilum RBL67 (RBL67), a human fecal isolate and health promoting candidate shows antagonistic and protective effects against Salmonella and Listeria spec. in vitro. However, the underlying mechanisms fostering these effects remain unknown. In this study, the interactions of RBL67 and Salmonella enterica subsp. enterica serovar Typhimurium N-15 (N-15) were explored by global transcriptional analysis. Results: Growth experiments were performed in a complex nutritive medium with controlled pH of 6.0 and suitable for balanced growth of both RBL67 and N-15. RBL67 growth was slightly enhanced in presence of N-15. Conversely, N-15 showed reduced growth in the presence of RBL67. Transcriptional analyses revealed higher expression of stress genes and amino acid related function in RBL67 in co-culture with N-15 when compared to mono-culture. Repression of the PhoP regulator was observed in N-15 in presence of RBL67. Further, RBL67 activated virulence genes located on the Salmonella pathogenicity islands 1 and 2. Flagellar genes, however, were repressed by RBL67. Sequential expression of flagellar, SPI 1 and fimbrial genes is essential for Salmonella infection. Our data revealed that RBL67 triggers expression of SPI 1 and fimbrial determinants prematurely, potentially leading to redundant energy expenditure. In the competitive environment of the gut such energy expenditure could lead to enhanced clearing of Salmonella. Conclusion: Our study provides first insights into probiotic-pathogen interactions on global transcriptional level and suggests that deregulation of virulence gene expression might be an additional protective mechanism of probiotica against infections of the host.
机译:背景:嗜热双歧杆菌RBL67(RBL67)是一种人类粪便分离物,具有促进健康的作用,对沙门氏菌和李斯特菌具有拮抗和保护作用。体外。但是,促进这些作用的潜在机制仍然未知。在这项研究中,RBL67和沙门氏菌亚种的相互作用。肠球菌血清鼠伤寒N-15(N-15)通过全局转录分析进行了探索。结果:生长实验在控制pH值为6.0且适合RBL67和N-15平衡生长的复杂营养培养基中进行。在N-15存在下,RBL67的生长略有增强。相反,在RBL67存在下,N-15的生长减少。转录分析显示,与单培养相比,在与N-15共培养的RBL67中,胁迫基因和氨基酸相关功能的表达更高。在存在RBL67的N-15中观察到PhoP调节剂的抑制。此外,RBL67激活了位于沙门氏菌致病岛1和2上的毒力基因。然而,鞭毛基因却被RBL67抑制。鞭毛,SPI 1和纤维基因的顺序表达对于沙门氏菌感染至关重要。我们的数据显示,RBL67过早触发SPI 1和纤维决定簇的表达,可能导致多余的能量消耗。在肠道的竞争环境中,这种能量消耗可能导致沙门氏菌的清除增加。结论:我们的研究提供了在全局转录水平上益生菌-病原体相互作用的初步见解,并表明解除毒力基因表达的调控可能是益生菌对抗宿主感染的另一种保护机制。

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