Evidence map›Paper›PMID 42769101›Full record

ArticleFrontiers in cellular and infection microbiology2026

Multi-omics profiling reveals microbiota-gut-brain axis dysregulation in an LPS-induced model of sepsis-associated encephalopathy.

Qi Shan, Ying Yu, Yongjie Zhang, Yiming Li, Jianqiang Zhang, Li Zhang, Qiang Liu, Hong Fu, Zhifeng Qu, Jiajia Duan and 1 more

Abstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Qi Shan *Department of Intensive Care Unit (Internal Medicine), The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Ying Yu *Department of Laboratory Medicine, First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yongjie Zhang *Department of Anesthesiology, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Yiming LiDepartment of Clinical Laboratory, The First Affiliated Hospital, College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Jianqiang ZhangDepartment of Intensive Care Unit (Internal Medicine), The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Li ZhangDepartment of Intensive Care Unit (Internal Medicine), The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Qiang LiuDepartment of Rehabilitation, The Third People's Provincial Hospital of Henan Province, Zhengzhou, China.
Hong FuDepartment of Rehabilitation, The Third People's Provincial Hospital of Henan Province, Zhengzhou, China.
Zhifeng QuDepartment of Medical Equipment, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Jiajia DuanDepartment of Clinical Laboratory, The First Affiliated Hospital, College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Qizhi FuDepartment of Intensive Care Unit (Internal Medicine), The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Sepsis-associated encephalopathy (SAE) is a common complication of sepsis. Its underlying mechanisms remain incompletely understood, and effective treatments are still lacking. Recent studies have shown that the microbiota-gut-brain axis may play a key role in the pathogenesis of SAE, but its potential mechanisms have not yet been clarified. Methods: In this study, we used a lipopolysaccharide (LPS)-induced zebrafish endotoxemia model and systematically characterized microbiota-gut-brain axis-associated alterations using multi-omics profiling combined with histopathology, behavioral assessment, and blood-brain barrier integrity assays. Results: Our results showed that LPS exposure induced intestinal inflammation and barrier disruption, neurovascular dysfunction, anxiety-like behavior, and impaired cognitive function in zebrafish. Gut microbiota profiling revealed marked compositional alterations, accompanied by widespread metabolic disturbances in intestinal and brain tissues. Brain transcriptomic analysis showed that the differentially expressed genes were closely associated with the PI3K-Akt signaling pathway, cell adhesion, and autophagy-related pathways. Cross-omics association analyses suggested potential associations among gut microbial dysbiosis, metabolic disturbances, and brain molecular responses. Conclusion: These findings suggest that disruption of the microbiota-gut-brain axis may contribute to LPS-induced SAE-like neurobehavioral abnormalities and provide a basis for further mechanistic and therapeutic studies.

Indexed as

BrainGastrointestinal MicrobiomeLipopolysaccharidesSepsis-Associated EncephalopathyAnimalsBlood-Brain BarrierDisease Models, AnimalDysbiosisEndotoxemiaGene Expression ProfilingMultiomicsSepsisZebrafishLipopolysaccharidesgut microbiotametabolomicsmicrobiota-gut-brain axissepsis-associated encephalopathytranscriptomicszebrafish

Identifiers

PMID42769101
PMCPMC13590405

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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.