Evidence map›Paper›PMID 42620267›Full record

ArticleFrontiers in cellular and infection microbiology2026

Multi-omics analysis reveals gut microbiota-host transcriptomic remodeling associated with the protective effects of Lacticaseibacillus rhamnosus GG against rotavirus enteritis.

Xiaoling Lin, Runjin Zhou, Bing Zhu, Haiyang He, Xiaogang Chen

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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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Xiaoling LinGuangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Runjin ZhouDongguan Hospital of Traditional Chinese Medicine, Dongguan, China.
Bing ZhuGuangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Haiyang HeDepartment of Immunology, Basic Medical School, Army Medical University (Third Military Medical University), Chongqin, China.
Xiaogang ChenThe First Affiliated Hospital, Guangzhou University of Traditional Chinese Medicine, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Rotavirus enteritis is closely associated with intestinal epithelial injury, gut microbial dysbiosis, and mucosal immune perturbation; however, the microbiota-host mechanisms underlying the protective effects of Lacticaseibacillus rhamnosus GG (LGG) remain incompletely defined. This study aimed to characterize LGG-induced microbiota-host transcriptomic remodeling in neonatal mice with rotavirus enteritis using an integrated multi-omics framework. Methods: BALB/c suckling mice were assigned to Control, Model, and LGG groups. Rotavirus enteritis was induced by oral gavage with SA11 rotavirus, and mice in the LGG group received oral LGG intervention for 7 consecutive days. Diarrhea symptoms and jejunal histopathological changes were evaluated. Gut microbial composition was analyzed using 16S rRNA sequencing, while jejunoileal transcriptional responses were profiled by RNA sequencing. Differentially abundant bacterial taxa, differentially expressed genes, KEGG-enriched pathways, mucosal B-cell/IgA-related transcriptional modules, and integrated Genus-Gene-Pathway networks were further analyzed. Results: LGG alleviated rotavirus-induced diarrhea, dehydration, body weight loss, and jejunal mucosal injury. Rotavirus infection disrupted the gut microbial ecosystem, with reduced α-diversity, altered community structure, increased Conclusion: LGG may promote the restoration of intestinal mucosal homeostasis after rotavirus infection by modulating coordinated changes between specific gut bacterial genera and host transcriptional programs related to mucosal repair and immune homeostasis. These findings provide integrated multi-omics evidence for microbiota-host interaction mechanisms underlying LGG-mediated protection against rotavirus enteritis.

Indexed as

EnteritisGastrointestinal MicrobiomeLacticaseibacillus rhamnosusRotavirus InfectionsTranscriptomeAnimalsAnimals, NewbornDisease Models, AnimalGene Expression ProfilingHost Microbial InteractionsIntestinal MucosaJejunumMiceMice, Inbred BALB CMultiomicsRNA, Ribosomal, 16SRNA, Ribosomal, 16Sgut microbiotaLacticaseibacillus rhamnosus GGmucosal immunitymulti-omicsrotavirus enteritistranscriptomics

Identifiers

PMID42620267
PMCPMC13485510

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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.