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益生菌混合物金双歧通过增强肠道防御预防新生儿 K1 移位。

Probiotic Mixture Golden Bifido Prevents Neonatal K1 Translocation via Enhancing Intestinal Defense.

作者信息

Zeng Qing, He Xiaolong, Puthiyakunnon Santhosh, Xiao Hansen, Gong Zelong, Boddu Swapna, Chen Lecheng, Tian Huiwen, Huang Sheng-He, Cao Hong

机构信息

Department of Microbiology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical UniversityGuangzhou, China.

The First School of Clinical Medicine, Southern Medical UniversityGuangzhou, China.

出版信息

Front Microbiol. 2017 Sep 20;8:1798. doi: 10.3389/fmicb.2017.01798. eCollection 2017.

DOI:10.3389/fmicb.2017.01798
PMID:28979247
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5611410/
Abstract

() K1 sepsis and meningitis is a severe infection characterized by high mortality in neonates. Successful colonization and translocation across the intestinal mucosa have been regarded as the critical steps for K1 sepsis and meningitis. We recently reported that the probiotic mixture, Golden Bifido (containing live , and , LBS) has a preventive role against neonatal K1 bacteremia and meningitis. However, the interaction between the neonatal gut barrier, probiotics and K1 is still not elucidated. The present study aims to investigate how LBS exerts its protective effects on neonatal gut barrier during K1 infection. The beneficial effects of LBS were explored and using human colon carcinoma cell lines HT-29 and rat model of neonatal K1 infection, respectively. Our results showed that stimulation with K1 was able to cause intestinal barrier dysfunction, which were reflected by K1-induced intestinal damage and apoptosis of intestinal epithelial cells, reduction of mucin, immunoglobulin A (IgA) and tight junction proteins expression, as well as increase in intestinal permeability, all these changes facilitate K1 intestinal translocation. However, these changes were alleviated when HT-29 cells were treated with LBS before K1 infection. Furthermore, we found that LBS-treated neonatal rats (without K1 infection) have showed higher production of mucin, ZO-1, IgA, Ki67 in intestinal mucosa as well as lower intestinal permeability than that of non-treated rats, indicating that LBS could accelerate the development of neonatal intestinal defense. Taken together, our results suggest that enhancement of the neonatal intestinal defense to fight against K1 translocation could be the potential mechanism to elucidate how LBS confers a protective effect against neonatal K1 bacteremia and meningitis. This indirect mechanism makes LBS exert preventive effect on most of gut-derived pathogenic infections rather than only .

摘要

()K1败血症和脑膜炎是一种严重感染,其特征是新生儿死亡率高。成功定植并穿过肠黏膜被认为是K1败血症和脑膜炎的关键步骤。我们最近报道,益生菌混合物金双歧(含有活的 、 和LBS)对新生儿K1菌血症和脑膜炎有预防作用。然而,新生儿肠道屏障、益生菌和K1之间的相互作用仍未阐明。本研究旨在探讨LBS在K1感染期间如何对新生儿肠道屏障发挥保护作用。分别使用人结肠癌细胞系HT-29和新生儿K1感染大鼠模型探索LBS的有益作用。我们的结果表明,K1刺激能够导致肠道屏障功能障碍,这表现为K1诱导的肠道损伤和肠上皮细胞凋亡、黏蛋白、免疫球蛋白A(IgA)和紧密连接蛋白表达减少,以及肠道通透性增加,所有这些变化都促进了K1的肠道易位。然而,在K1感染前用LBS处理HT-29细胞时,这些变化得到了缓解。此外,我们发现用LBS处理的新生大鼠(未感染K1)与未处理的大鼠相比,肠黏膜中黏蛋白、ZO-1、IgA、Ki67的产生更高,肠道通透性更低,表示LBS可以加速新生儿肠道防御的发育。综上所述,我们的结果表明,增强新生儿肠道防御以对抗K1易位可能是阐明LBS如何对新生儿K1菌血症和脑膜炎发挥保护作用的潜在机制。这种间接机制使LBS对大多数源自肠道的致病性感染发挥预防作用,而不仅仅是对 。

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