ArticleThe Journal of biological chemistry2010
TRIF mediates Toll-like receptor 5-induced signaling in intestinal epithelial cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 93 citations in OpenAlex.
- Review
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- Role of pattern recognition receptors and microbiota-derived ligands in obesity.Frontiers in microbiomes · 2024Review
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- Impact of Functional Polymorphisms on Drug Survival of Biological Therapies in Patients with Moderate-to-Severe Psoriasis.International journal of molecular sciences · 2023Observational
- TLR5-Derived, TIR-Interacting Decoy Peptides to Inhibit TLR Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Know your neighbors: microbial recognition at the intestinal barrier and its implications for gut homeostasis and inflammatory bowel disease.Frontiers in cell and developmental biology · 2023Review
- TIRAP, TRAM, and Toll-Like Receptors: The Untold Story.Mediators of inflammation · 2023Review
- Influence of Genetic Polymorphisms on Response to Biologics in Moderate-to-Severe Psoriasis.Journal of personalized medicine · 2021Review
- Impact of Interleukin 10 Deficiency on Intestinal Epithelium Responses to Inflammatory Signals.Frontiers in immunology · 2021Article
- Crosstalk Between Intestinal Serotonergic System and Pattern Recognition Receptors on the Microbiota-Gut-Brain Axis.Frontiers in endocrinology · 2021Review
- Flagellin-Stimulated Production of Interferon-β Promotes Anti-Flagellin IgG2c and IgA Responses.Molecules and cells · 2020Article
- Comparative Transcriptome Analysis Provides Insights into the Polyunsaturated Fatty Acid Synthesis Regulation ofInternational journal of molecular sciences · 2020Article
- Article
- Beyond defense: regulation of neuronal morphogenesis and brain functions via Toll-like receptors.Journal of biomedical science · 2019Review
- Pten gene deletion in intestinal epithelial cells enhances susceptibility to Salmonella Typhimurium infection in mice.Journal of microbiology (Seoul, Korea) · 2019Article
- Dynamic Gene Network Analysis of Caco-2 Cell Response to Shiga Toxin-ProducingMicroorganisms · 2019Article
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- Functional expression of TLR5 of different vertebrate species and diversification in intestinal pathogen recognition.Scientific reports · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Toll-like receptors (TLRs) associate with adaptor molecules (MyD88, Mal/TIRAP, TRAM, and TRIF) to mediate signaling of host-microbial interaction. For instance, TLR4 utilizes the combination of both Mal/TIRAP-MyD88 (MyD88-dependent pathway) and TRAM-TRIF (MyD88-independent pathway). However, TLR5, the specific receptor for flagellin, is known to utilize only MyD88 to elicit inflammatory responses, and an involvement of other adaptor molecules has not been suggested in TLR5-dependent signaling. Here, we found that TRIF is involved in mediating TLR5-induced nuclear factor κB (NFκB) and mitogen-activated protein kinases (MAPKs), specifically JNK1/2 and ERK1/2, activation in intestinal epithelial cells. TLR5 activation by flagellin permits the physical interaction between TLR5 and TRIF in human colonic epithelial cells (NCM460), whereas TLR5 does not interact with TRAM upon flagellin stimulation. Both primary intestinal epithelial cells from TRIF-KO mice and TRIF-silenced NCM460 cells significantly reduced flagellin-induced NFκB (p105 and p65), JNK1/2, and ERK1/2 activation compared with control cells. However, p38 activation by flagellin was preserved in these TRIF-deficient cells. TRIF-KO intestinal epithelial cells exhibited substantially reduced inflammatory cytokine (keratinocyte-derived cytokine, macrophage inflammatory protein 3α, and IL-6) expression upon flagellin, whereas control cells from TRIF-WT mice showed robust cytokine expression by flagellin. Compare with TRIF-WT mice, TRIF-KO mice were resistant to in vivo intestinal inflammatory responses: flagellin-mediated exacerbation of colonic inflammation and dextran sulfate sodium-induced experimental colitis. We conclude that in addition to MyD88, TRIF mediates TLR5-dependent responses and, thereby regulates inflammatory responses elicited by flagellin/TLR5 engagement. Our findings suggest an important role of TRIF in regulating host-microbial communication via TLR5 in the gut epithelium.
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