Kimball1, J., Nittayananta1, W., Klausner4, M., Chung1, W., Dale1,2,3, B. 1Department of Oral Biology, University of Washington, 2Department of Medicine/Dermatology, University of Washington, 3Department of Biochemistry, University of Washington, 4The MatTek Corporation, Ashland, MA. Arch.

This study by researchers at the University of Washington demonstrated that MatTek’s EpiOral human buccal tissue equivalent has an in vivo-like antimicrobial barrier and is therefore a superior in vitro model of oral epithelia when compared to submerged monolayer cell cultures. Objective: Oral epithelia function as a microbial barrier and are actively involved in recognizing and responding to bacteria. In this study, the objective of researchers at the University of Washington was to examine MatTek’s EpiOral™, a tissue engineered model of buccal epithelium, for its response to oral bacteria and proinflammatory cytokines and compare the EpiOral tissue responses with those of a submerged monolayer cell culture. Design: The EpiOral tissue model was characterized for keratin and b-defensin expression. Altered expression of b-defensins was evaluated by RT-PCR after exposure of the apical surface to oral bacteria and after exposure to TNF-a in the medium. The EpiOral responses were compared to the response in traditional submerged oral epithelial cell culture. Results: The EpiOral buccal model showed expression of differentiation specific keratin 13, hBD1 and hBD3 in the upper half of the tissue; hBD2 was not detected. hBD1 mRNA was constitutively expressed, while hBD2 mRNA increased 2-fold after exposure of the apical surface to three oral bacteria tested and hBD3 mRNA increased in response to the non-pathogenic bacteria tested. In contrast, hBD2 mRNA increased 3—600-fold in response to bacteria in submerged cell culture. HBD2 mRNA increased over 100-fold in response to TNF-a in the EpiOral tissue model and 50-fold in submerged cell culture. Thus, the EpiOral tissue model is capable of up-regulating hBD2, however, the minimal response to bacteria suggests that the EpiOral tissue has an effective antimicrobial barrier due to its morphology, differentiation, and defensin expression. Conclusions: The EpiOral oral mucosal model is differentiated, expresses hBD1 and hBD3, and has an intact surface with a functional antimicrobial barrier.


Beta-defensins, Buccal mucosa, Commensal bacteria, EpiOral, Extracellular matrix, Fusobacterium nucleatum ATCC 25586, GAPDH, Gram-negative bacteria, Human beta-defensin 1 (hBD1), Human beta-defensin 2 (hBD2), Human beta-defensin 3 (hBD3), IL-8, Keratin 13, Keratin 14, Microbial barrier , Normal human oral keratinocytes, ORL-100, Oral cavity, PAR 1, PAR 2, Pathogenic bacteria, Porphyromonas gingivalis, Proinflammatory cytokines , Rabbit polyclonal antibodies , Ribosomal phosphoprotein (RPO), Streptococcus gordonii, Toll like receptors 2 (TLR 2), Toll like receptors 4 (TLR 4)

Materials Tested

EpiOral, Fusobacterium nucleatum ATCC 25586, IL-1b, Normal human oral keratinocytes, ORL-100, Porphyromonas gingivalis, Streptococcus gordonii, TNF-a

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