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LI05对小鼠模型感染的保护作用

Protective Effect of LI05 Against Infection in a Mouse Model.

作者信息

Xu Qiaomai, Gu Silan, Chen Yunbo, Quan Jiazheng, Lv Longxian, Chen Dazhi, Zheng Beiwen, Xu Lichen, Li Lanjuan

机构信息

State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

出版信息

Front Microbiol. 2018 Oct 9;9:2396. doi: 10.3389/fmicb.2018.02396. eCollection 2018.

DOI:10.3389/fmicb.2018.02396
PMID:30356740
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6189400/
Abstract

infection (CDI) is a major cause of infectious diarrhea among hospitalized patients. Probiotics could be instrumental in restoring the intestinal dysbiosis caused by CDI. Here, we examined the protective effect of LI05 in a mouse CDI model. C57BL/6 mice were administrated LI05 (LI05 group) or sterile anaerobic PBS (CDI group) everyday for 14 days. Mice were exposed to antibiotics cocktail for 5 days; then challenged with strain VPI10463. Mice were monitored daily for survival and weight loss. Colonic tissue and serum samples were assessed for intestinal histopathology, intestinal barrier function and systemic inflammation. The oral administration of LI05 improved the survival rate and alleviated the histopathological impact of . Compared to the CDI group, the levels of inflammatory mediators in the colon as well as inflammatory cytokines and chemokines in serum were substantially attenuated in the LI05 group. LI05 alleviated the CDI-induced of disruption of ZO-1, occludin and claudin-1. Additionally, fecal microbiome analysis showed an enrichment in the abundance of the and , while, the relative abundance of were decreased. Our results demonstrated that the preventive effect of LI05 against CDI was mediated via improving tight junction proteins and down-regulating the inflammatory response. Therefore, LI05 could be a promising probiotic in CDI.

摘要

艰难梭菌感染（CDI）是住院患者感染性腹泻的主要原因。益生菌可能有助于恢复由CDI引起的肠道菌群失调。在此，我们在小鼠CDI模型中研究了LI05的保护作用。将C57BL/6小鼠每天给予LI05（LI05组）或无菌厌氧PBS（CDI组），持续14天。小鼠接受抗生素鸡尾酒处理5天；然后用VPI10463菌株进行攻击。每天监测小鼠的存活情况和体重减轻情况。评估结肠组织和血清样本的肠道组织病理学、肠道屏障功能和全身炎症。口服LI05提高了存活率并减轻了[未明确的相关影响]的组织病理学影响。与CDI组相比，LI05组结肠中炎症介质以及血清中炎症细胞因子和趋化因子的水平显著降低。LI05减轻了CDI诱导的紧密连接蛋白ZO-1、闭合蛋白和Claudin-1的破坏。此外，粪便微生物组分析显示[未明确的相关菌属]丰度增加，而[未明确的相关菌属]的相对丰度降低。我们的结果表明，LI05对CDI的预防作用是通过改善紧密连接蛋白和下调炎症反应介导的。因此，LI05可能是一种有前途的用于CDI的益生菌。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/7dee696d8850/fmicb-09-02396-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/385181d71e5b/fmicb-09-02396-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/3a2e7729e497/fmicb-09-02396-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/3f6d49f509b2/fmicb-09-02396-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/6426b797784d/fmicb-09-02396-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/d6daeb55bb96/fmicb-09-02396-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/7dee696d8850/fmicb-09-02396-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/385181d71e5b/fmicb-09-02396-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/3a2e7729e497/fmicb-09-02396-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/3f6d49f509b2/fmicb-09-02396-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/6426b797784d/fmicb-09-02396-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/d6daeb55bb96/fmicb-09-02396-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83f1/6189400/7dee696d8850/fmicb-09-02396-g006.jpg

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