ArticleThe Journal of biological chemistry2010
Fusobacterium nucleatum-associated beta-defensin inducer (FAD-I): identification, isolation, and functional evaluation.
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 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- Microbiota in cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Article
- Assays with Patient-Derived Organoids to Evaluate the Impact of Microbial Infection on Base Excision Repair (BER) Enzymes.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Pathogenic Mechanisms ofFrontiers in oral health · 2022Review
- Review
- Role of FAD-I in Fusobacterial Interspecies Interaction and Biofilm Formation.Microorganisms · 2020Article
- Article
- Article
- Conceptual Perspectives: Bacterial Antimicrobial Peptide Induction as a Novel Strategy for Symbiosis with the Human Host.Frontiers in microbiology · 2018Article
- A chemical and biological toolbox for Type Vd secretion: Characterization of the phospholipase A1 autotransporter FplA fromThe Journal of biological chemistry · 2017Article
- Target identification in Fusobacterium nucleatum by subtractive genomics approach and enrichment analysis of host-pathogen protein-protein interactions.BMC microbiology · 2016Article
- FAD-I, a Fusobacterium nucleatum Cell Wall-Associated Diacylated Lipoprotein That Mediates Human Beta Defensin 2 Induction through Toll-Like Receptor-1/2 (TLR-1/2) and TLR-2/6.Infection and immunity · 2016Article
- Fusobacterium nucleatum: a commensal-turned pathogen.Current opinion in microbiology · 2015Review
- Epithelial innate immune response to Acinetobacter baumannii challenge.Infection and immunity · 2014Article
- LL-37 opsonizes and inhibits biofilm formation of Aggregatibacter actinomycetemcomitans at subbactericidal concentrations.Infection and immunity · 2013Article
- Defensins and LL-37: a review of function in the gingival epithelium.Periodontology 2000 · 2013Review
- Comparison of epigenetic profiles of human oral epithelial cells from HIV-positive (on HAART) and HIV-negative subjects.Epigenetics · 2013Article
- The antibacterial activity of LL-37 against Treponema denticola is dentilisin protease independent and facilitated by the major outer sheath protein virulence factor.Infection and immunity · 2012Article
- The yin and yang of human Beta-defensins in health and disease.Frontiers in immunology · 2012Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Human β-defensins (hBDs) are small, cationic antimicrobial peptides, secreted by mucosal epithelial cells that regulate adaptive immune functions. We previously reported that Fusobacterium nucleatum, a ubiquitous gram-negative bacterium of the human oral cavity, induces human β-defensin 2 (hBD2) upon contact with primary oral epithelial cells. We now report the isolation and characterization of an F. nucleatum (ATCC 25586)-associated defensin inducer (FAD-I). Biochemical approaches revealed a cell wall fraction containing four proteins that stimulated the production of hBD2 in human oral epithelial cells (HOECs). Cross-referencing of the N-terminal sequences of these proteins with the F. nucleatum genome revealed that the genes encoding the proteins were FadA, FN1527, FN1529, and FN1792. Quantitative PCR of HOEC monolayers challenged with Escherichia coli clones expressing the respective cell wall proteins revealed that FN1527 was most active in the induction of hBD2 and hence was termed FAD-I. We tagged FN1527 with a c-myc epitope on the C-terminal end to identify and purify it from the E. coli clone. Purified FN1527 (FAD-I) induced hBD2 mRNA and protein expression in HOEC monolayers. F. nucleatum cell wall and FAD-I induced hBD2 via TLR2. Porphorymonas gingivalis, an oral pathogen that does not induce hBD2 in HOECs, was able to significantly induce expression of hBD2 in HOECs only when transformed to express FAD-I. FAD-I or its derivates offer a potentially new paradigm in immunoregulatory therapeutics because they may one day be used to bolster the innate defenses of vulnerable mucosae.
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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.