ArticleClinical and experimental immunology2022
The mechanism on Prevotella melaninogenica promoting the inflammatory progression of oral lichen planus.
Article in Clinical and experimental immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Exploring the Diagnostic and Predictive Value of Oral Microbiome in Esophageal Cancer: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2025Pooled it
- Aberrant Accumulation of Cell-Free DNA Activates the cGAS-STING-TBK1 Pathway of γδ T Cells to Promote the Inflammatory Responses in Oral Lichen Planus.Inflammation · 2026Article
- Microbiome and metabolome integrated analysis reveals oral microbiota alterations and associated metabolic pathways in allergic rhinitis.Journal of oral microbiology · 2026Article
- Filtration-enriched metabolites and their association with salivary microbiota: a combined two-cohort analysis.Journal of oral microbiology · 2026Article
- Microbial dysbiosis in oral cavity determines obesity status in adolescents.Cellular and molecular life sciences : CMLS · 2025Article
- Exploring the oral bacteria-oral lichen planus connection: mechanisms, clinical implications and future directions.Archives of microbiology · 2025Review
- The Role of TRPV1/CGRP Pathway Activated byInternational journal of molecular sciences · 2025Article
- Fraxin alleviates oral lichen planus by suppressing OCT3-mediated activation of FGF2/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Associations of Chronic Marijuana Use with Changes in Salivary Microbiome.Microorganisms · 2024Article
- Article
- Roles of intralesional bacteria in the initiation and progression of oral squamous cell carcinoma.Cancer medicine · 2024Review
- Oral Microbiota Alterations in Subjects with SARS-CoV-2 Displaying Prevalence of the Opportunistic Fungal PathogenMicroorganisms · 2024Article
- FloxedCells · 2024Article
- Bibliometric analysis of recent research on the association between TRPV1 and inflammation.Channels (Austin, Tex.) · 2023Article
- Identification of proteotoxic and proteoprotective bacteria that non-specifically affect proteins associated with neurodegenerative diseases.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oral lichen planus (OLP) is a common chronic inflammatory disease occurring in the oral mucosa. Bacteria are a key driver of mucosal immune responses and can induce changes in gene expression and function of epithelial keratinocytes. IL-36γ can induce the expression of antimicrobial peptides, cytokines, and chemokines, and is widely involved in many chronic inflammatory diseases. Our aim is to explore the role of IL-36γ in the pathological process of OLP when Prevotella melaninogenica (P. melaninogenica) invades the oral mucosa. The expression of IL-36γ in OLP lesions and mice was detected by immunohistochemistry. Recombinant human IL-36Gamma (rhIL-36γ) was used to treat oral keratinocytes and the expression levels of inflammatory cytokines were detected by qRT-PCR and ELISA. The expression of IL-36γ and TRPV1 was detected by western blotting following co-culturing P. melaninogenica with oral keratinocytes. The mRNA expression of IL-36γ was detected by qRT-PCR. From our results, IL-36γ was upregulated in OLP lesions. Exogenous rhIL-36γ promoted the expression of pro-inflammatory cytokines and antibacterial peptides in oral keratinocytes. The expression of IL-36γ was significantly increased following the stimulation of P. melaninogenica in oral keratinocytes and mice. TRPV1 activation was induced by P. melaninogenica and its activation enhanced the expression of IL-36γ. IL-36Ra could reduce the inflammation in OLP in vitro. In summary, overexpression of IL-36γ in OLP lesions could promote its pathogenesis by inducing inflammation. P. melaninogenica invasion of oral keratinocytes could induce the expression of IL-36γ by the activation of TRPV1, thereby regulating the interaction between bacteria and oral epithelial cells.
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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.