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423 和 ST4SA 抗李斯特菌活性的机制:细菌素产生和黏附特性。

Bacteriocin production and adhesion properties as mechanisms for the anti-listerial activity of 423 and ST4SA.

机构信息

1 Department of Microbiology, University of Stellenbosch, Matieland, Stellenbosch 7600, South Africa.

出版信息

Benef Microbes. 2019 Apr 19;10(3):329-349. doi: 10.3920/BM2018.0141. Epub 2019 Feb 18.

Abstract

Probiotics play an important role in maintaining a healthy and stable intestinal microbiota, primarily by preventing infection. Probiotic lactic acid bacteria (LAB) are known to be inhibitory to many bacterial enteric pathogens, including antibiotic-resistant strains. Whilst the positive role that probiotics have on human physiology, specifically in the treatment or prevention of specific infectious diseases of the gastro-intestinal tract (GIT) is known, the precise mechanistic basis of these effects remains a major research goal. In this study, molecular evidence to underpin the protective and anti-listerial effect of 423 and ST4SA against orally administered EGDe in the GIT of mice is provided. Bacteriocins plantaricin 423 and mundticin ST4SA, produced by 423 and ST4SA, respectively, inhibited the growth of and . Bacteriocin-negative mutants of 423 and ST4SA failed to exclude EGDe from the gastrointestinal tract (GIT) of mice. Furthermore, 423 and ST4SA failed to inhibit recombinant strains of EGDe that expressed the immunity proteins of the two bacteriocins. These results confirmed that bacteriocins plantaricin 423 and mundticin ST4SA acted as anti-infective mediators . Compared to wild type strains, mutants of 423 and ST4SA, in which the adhesion genes were knocked out, were less effective in the exclusion of EGDe from the GIT of mice. This work demonstrates the importance of bacteriocin and adhesion genes as probiotic anti-infective mechanisms.

摘要

益生菌在维持健康稳定的肠道微生物群方面发挥着重要作用,主要通过预防感染来实现。众所周知,益生菌乳酸菌(LAB)对许多肠道病原体具有抑制作用,包括抗生素耐药菌株。虽然益生菌对人体生理学,特别是在治疗或预防胃肠道(GIT)特定感染性疾病方面的积极作用是已知的,但这些作用的确切机制基础仍然是一个主要的研究目标。在这项研究中,提供了支持 423 和 ST4SA 对口服给予 GIT 中的 EGDe 的保护和抗李斯特菌作用的分子证据。由 423 和 ST4SA 分别产生的细菌素 plantaricin 423 和 mundticin ST4SA 抑制了 和 的生长。423 和 ST4SA 的细菌素阴性突变体未能将 EGDe 从胃肠道(GIT)中排除。此外,423 和 ST4SA 未能抑制表达两种细菌素免疫蛋白的重组 EGDe 菌株。这些结果证实了细菌素 plantaricin 423 和 mundticin ST4SA 作为抗感染介质发挥作用。与野生型菌株相比,缺失了粘附基因的 423 和 ST4SA 突变体在将 EGDe 从 GIT 中排除方面的效果较差。这项工作证明了细菌素和粘附基因作为益生菌抗感染机制的重要性。

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