Evidence map›Paper›PMID 38369503›Full record

ArticleJournal of translational medicine2024

Autoinducer-2 promotes the colonization of Lactobacillus rhamnosus GG to improve the intestinal barrier function in a neonatal mouse model of antibiotic-induced intestinal dysbiosis.

Riqiang Hu, Ting Yang, Qing Ai, Yuan Shi, Yanchun Ji, Qian Sun, Bei Tong, Jie Chen, Zhengli Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.1field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 22 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Riqiang HuChildren Nutrition Research Center, Chongqing Key Laboratory of Child Neurodevelopmental and Cognitive Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Chongqing, China.
Ting YangChildren Nutrition Research Center, Chongqing Key Laboratory of Child Neurodevelopmental and Cognitive Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Chongqing, China.
Qing AiDepartment of Neonatology, National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Yuan ShiDepartment of Neonatology, National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Yanchun JiDepartment of Neonatology, National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Qian SunDepartment of Neonatology, National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Bei TongChildren Nutrition Research Center, Chongqing Key Laboratory of Child Neurodevelopmental and Cognitive Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Chongqing, China.
Jie ChenChildren Nutrition Research Center, Chongqing Key Laboratory of Child Neurodevelopmental and Cognitive Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Chongqing, China. jchen010@hospital.cqmu.edu.cn.
Zhengli WangChildren Nutrition Research Center, Chongqing Key Laboratory of Child Neurodevelopmental and Cognitive Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Chongqing, China. zhengli_wang@126.com.
Children's Hospital of Chongqing Medical University · CNChongqing Medical University · CN

Funding

National Key Research and Development Program of China 2022YFC2704802National Science Foundation of China 31971089the fellowship of China Postdoctoral Science Foundation 2022MD713716the Science and Technology Research Program of Chongqing Municipal Education Commission KJQN202200414the Scientific Research Foundation of the Science and Technology Commission of Chongqing CSTB2023NSCQ-MSX0178
6 · The paper itself

Abstract

backgroundHuman health is seriously threatened by antibiotic-induced intestinal disorders. Herein, we aimed to determine the effects of Autoinducer-2 (AI-2) combined with Lactobacillus rhamnosus GG (LGG) on the intestinal barrier function of antibiotic-induced intestinal dysbiosis neonatal mice.

methodsAn antibiotic-induced intestinal dysbiosis neonatal mouse model was created using antibiotic cocktails, and the model mice were randomized into the control, AI-2, LGG, and LGG + AI-2 groups. Intestinal short-chain fatty acids and AI-2 concentrations were detected by mass spectrometry and chemiluminescence, respectively. The community composition of the gut microbiota was analyzed using 16S rDNA sequencing, and biofilm thickness and bacterial adhesion in the colon were assessed using scanning electron microscopy. Transcriptome RNA sequencing of intestinal tissues was performed, and the mRNA and protein levels of HCAR2 (hydroxycarboxylic acid receptor 2), claudin3, and claudin4 in intestinal tissues were determined using quantitative real-time reverse transcription PCR and western blotting. The levels of inflammatory factors in intestinal tissues were evaluated using enzyme-linked immunosorbent assays (ELISAs). D-ribose, an inhibitor of AI-2, was used to treat Caco-2 cells in vitro.

resultsCompared with the control, AI-2, and LGG groups, the LGG + AI-2 group showed increased levels of intestinal AI-2 and proportions of Firmicutes and Lacticaseibacillus, but a reduced fraction of Proteobacteria. Specifically, the LGG + AI-2 group had considerably more biofilms and LGG on the colon surface than those of other three groups. Meanwhile, the combination of AI-2 and LGG markedly increased the concentration of butyric acid and promoted Hcar2, claudin3 and claudin4 expression levels compared with supplementation with LGG or AI-2 alone. The ELISAs revealed a significantly higher tumor necrosis factor alpha (TNF-α) level in the control group than in the LGG and LGG + AI-2 groups, whereas the interleukin 10 (IL-10) level was significantly higher in the LGG + AI-2 group than in the other three groups. In vitro, D-ribose treatment dramatically suppressed the increased levels of Hcar2, claudin3, and claudin4 in Caco-2 cells induced by AI-2 + LGG.

conclusionsAI-2 promotes the colonization of LGG and biofilm formation to improve intestinal barrier function in an antibiotic-induced intestinal dysbiosis neonatal mouse model.

Indexed as

Lacticaseibacillus rhamnosusProbioticsAnimalsAnimals, NewbornAnti-Bacterial AgentsCaco-2 CellsClaudin-4DysbiosisHumansIntestinal Barrier FunctionMiceRiboseAnti-Bacterial AgentsClaudin-4RiboseAntibiotics-induced intestinal floraAutoinducer-2BiofilmButyric acidHydroxycarboxylic acid receptor 2Intestinal barrier functionLactobacillus rhamnosus GGTight junctions

Identifiers

PMID38369503
PMCPMC10874557
OpenAlexW4391918987

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.