ArticlePLoS pathogens2022
Insight into mechanisms of pig lncRNA FUT3-AS1 regulating E. coli F18-bacterial diarrhea.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- Exosomal circRNA Transcriptome Analysis of Porcine Intestinal Epithelial Cells UnderAnimals : an open access journal from MDPI · 2026Article
- Review
- Transcriptomics-based investigation of resistance differences to swine fever between large white pigs and min pigs.Virus research · 2025Article
- Unveiling the Hidden Regulators: The Impact of lncRNAs on Zoonoses.International journal of molecular sciences · 2024Review
- Identification cloning and functional analysis of novel natural antisense lncRNA CFL1-AS1 in cattle.Epigenetics · 2023Article
- Article
- Article
- METTL3-Mediated LncRNAInternational journal of molecular sciences · 2023Article
- Effect and Mechanism Analysis of PigInternational journal of molecular sciences · 2022Article
- Expression Analysis and the Roles of theGenes · 2022Article
- LncRNAFrontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Escherichia coli F18 is a common conditional pathogen that is associated with a variety of infections in humans and animals. LncRNAs have emerged as critical players in pathogen infection, but their role in the resistance of the host to bacterial diarrhea remains unknown. Here, we used piglets as animal model and identified an antisense lncRNA termed FUT3-AS1 as a host regulator related to E. coli F18 infection by RNA sequencing. Downregulation of FUT3-AS1 expression contributed to the enhancement of E. coli F18 resistance in IPEC-J2 cells. FUT3-AS1 knockdown reduced FUT3 expression via decreasing the H4K16ac level of FUT3 promoter. Besides, the FUT3-AS1/miR-212 axis could act as a competing endogenous RNA to regulate FUT3 expression. Functional analysis demonstrated that target FUT3 plays a vital role in the resistance of IPEC-J2 cells to E. coli F18 invasion. A Fut3-knockout mice model was established and Fut3-knockout mice obviously improved the ability of resistance to bacterial diarrhea. Interestingly, FUT3 could enhance E. coli F18 susceptibility by activating glycosphingolipid biosynthesis and toll-like receptor signaling which are related to receptor formation and immune response, respectively. In summary, we have identified a novel biomarker FUT3-AS1 that modulates E. coli F18 susceptibility via histone H4 modifications or miR-212/FUT3 axis, which will provide theoretical guidance to develop novel strategies for combating bacterial diarrhea in piglets.
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Registered trials
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