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肠球菌的肠道易位需要肠腔内肠球菌过度生长达到一个阈值水平。

Intestinal translocation of enterococci requires a threshold level of enterococcal overgrowth in the lumen.

机构信息

Micalis Institute, INRA, AgroParisTech, Université Paris-Saclay, 78350, Jouy en Josas, France.

出版信息

Sci Rep. 2019 Jun 20;9(1):8926. doi: 10.1038/s41598-019-45441-3.

DOI:10.1038/s41598-019-45441-3
PMID:31222056
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6586816/
Abstract

Enterococci are subdominant members of the human gastrointestinal microbiota. Enterococcus faecalis is generally harmless for healthy individuals, but it can cause a diverse range of infections in immunodeficient or elderly patients with severe underlying diseases. In this study, we analysed the levels of intestinal translocation of indigenous enterococci in C57BL/6, CF-1 and CX3CR1 mice upon clindamycin antibiotic-induced dysbiosis. We found that C57BL/6 was the most permissive model for enterococcal translocation and that initiation of E. faecalis translocation coincided with a threshold of enterococcal colonisation in the gut lumen, which once reached, triggered E. faecalis dissemination to deeper organs. We showed that the extent to which E. faecalis clinical strain VE14821 competed with indigenous enterococci differed between the C57BL/6 and CX3CR1 models. Finally, using a simplified gnotobiotic model, we observed E. faecalis crossing an intact intestinal tract using intestinal epithelial cells as one route to reach the lamina propria. Our study opens new perspectives for assessing the effect of various immunodeficiencies and for investigating mechanisms underlying enterococcal translocation.

摘要

肠球菌是人类胃肠道微生物群中的亚优势成员。粪肠球菌通常对健康个体无害,但它可导致免疫缺陷或患有严重基础疾病的老年患者发生各种感染。在这项研究中,我们分析了克林霉素抗生素诱导的肠道菌群失调后,C57BL/6、CF-1 和 CX3CR1 小鼠中内源性肠球菌的肠道易位水平。我们发现 C57BL/6 是肠球菌易位最易发生的模型,并且 E. faecalis 易位的开始与肠道腔中肠球菌定植的阈值相吻合,一旦达到该阈值,就会引发 E. faecalis 向更深层器官的传播。我们表明,临床分离株 VE14821 与内源性肠球菌竞争的程度在 C57BL/6 和 CX3CR1 模型之间有所不同。最后,我们使用简化的无菌动物模型观察到 E. faecalis 通过肠上皮细胞作为到达固有层的一种途径穿过完整的肠道。我们的研究为评估各种免疫缺陷的影响以及研究肠球菌易位的机制开辟了新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6305/6586816/97e340f52fa9/41598_2019_45441_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6305/6586816/a2379f5c6bfc/41598_2019_45441_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6305/6586816/b6b3e08fdb5b/41598_2019_45441_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6305/6586816/3f72c5147bfd/41598_2019_45441_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6305/6586816/0115a34e8168/41598_2019_45441_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6305/6586816/97e340f52fa9/41598_2019_45441_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6305/6586816/a2379f5c6bfc/41598_2019_45441_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6305/6586816/b6b3e08fdb5b/41598_2019_45441_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6305/6586816/3f72c5147bfd/41598_2019_45441_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6305/6586816/0115a34e8168/41598_2019_45441_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6305/6586816/97e340f52fa9/41598_2019_45441_Fig5_HTML.jpg

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