ArticleCytokine2018
Recognition of Candida albicans by gingival fibroblasts: The role of TLR2, TLR4/CD14, and MyD88.
Article in Cytokine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Matrix Stiffness Governs Fibroblasts' Regulation of Gingival Immune Homeostasis.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Matrix Stiffness Governs Fibroblast-Driven Immune Homeostasis in Gingival Tissues.bioRxiv : the preprint server for biology · 2025Article
- The role of nucleic acid sensors in antifungal immunity.Frontiers in immunology · 2025Review
- TLR2 promotes traumatic deep venous thrombosis of the lower extremity following femoral fracture by activating the NF‑κB/COX‑2 signaling pathway in rats.Experimental and therapeutic medicine · 2024Article
- Itraconazole-Loaded Ufasomes: Evaluation, Characterization, and Anti-Fungal Activity againstPharmaceutics · 2022Article
- Expression of anti-fungal peptide, β-defensin 118 in oral fibroblasts induced by C. albicans β-glucan-containing particles.Journal of applied oral science : revista FOB · 2022Article
- Fungi-A Component of the Oral Microbiome Involved in Periodontal Diseases.Advances in experimental medicine and biology · 2022Article
- In vitro and in vivo study of the pathogenic role of PPARα in experimental periodontitis.Journal of applied oral science : revista FOB · 2022Article
- Article
- Polymorphism of CD14 Gene Is Associated with Adverse Outcome among Patients Suffering from Cardiovascular Disease.Mediators of inflammation · 2021Observational
- Review
- Recognition ofMicroorganisms · 2020Review
- Article
- Expression of toll-like receptors and their regulatory roles in murine cardiac telocytes.Journal of cellular and molecular medicine · 2019Article
- Review
- TLR2 deficiency enhances susceptibility to oral carcinogenesis by promoting an inflammatory environment.American journal of cancer research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Recent evidence indicates that nonprofessional immune cells such as epithelial cells, endothelial cells, and fibroblasts also contribute to innate immunity via secretion of cytokines. Fibroblasts are the principal type of cell found in the periodontal connective tissues and they are involved in the immune response during periodontal disease. The role of fibroblasts in the recognition of pathogens via Toll-like receptors (TLRs) has been established; however, few studies have been conducted concerning the involvement of innate immune receptors in the recognition of Candida albicans by gingival fibroblast. In the current study, we investigate the functional activity of TLR2, cluster of differentiation 14 (CD14), and myeloid differentiation primary response gene 88 (MyD88) molecules in the recognition of C. albicans by gingival fibroblast. First, we identified that gingival fibroblasts expressed TLR2, TLR3, and TLR4. Our results showed that TLR agonists had no effect on these receptors' expression by TLR2, MyD88, and CD14-deficient cells. Notably, C. albicans and a synthetic triacylated lipoprotein (Pam3CSK4) induced a remarkable increase of TLR3 expression on MyD88-deficient gingival fibroblasts. TLR4 expression levels were lower than TLR2 and TLR3 levels and remained unchanged after TLR agonist stimulation. Gingival fibroblasts presented morphological similarities; however, TLR2 deficiency on these cells leads to a lower proliferative response, whereas the deficiency on CD14 expression resulted in lower levels of type I collagen by these cells. In addition, the recognition of C. albicans by gingival fibroblasts had an effect on the secretion of cytokines and it was dependent on a specific recognition molecule. Specifically, tumor necrosis factor-α (TNF-α) production after the recognition of C. albicans was dependent on MyD88, CD14, and TLR2 molecules, whereas the production of interleukin-1β (IL-1β) and IL-13 was dependent on TLR2. These findings are the first to describe a role of gingival fibroblast in the recognition of C. albicans and the pathways involved in this process. An understanding of these pathways may lead to alternative treatments for patients with periodontal disease.
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Registered trials
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.