Abstract
Periodontal diseases initiate on epithelial surfaces of the subgingival compartment, while the gingival epithelium functions as an epithelial barrier against microbial infection and orchestrates immune responses. Porphyromonas gingivalis is a major pathogen of periodontal diseases and has an ability to penetrate the epithelial barrier. To assess the molecular basis of gingival epithelial barrier dysfunction associated with P. gingivalis, we newly developed a three-dimensional multilayered tissue model of gingival epithelium with gene manipulation. Using this novel approach, P. gingivalis gingipains including Arg- or Lys-specific cysteine proteases were found to specifically degrade junctional adhesion molecule 1 and coxsackievirus and adenovirus receptor in the tissue model, leading to increased permeability for lipopolysaccharide, peptidoglycan, and gingipains. This review summarizes the strategy used by P. gingivalis to disable the epithelial barrier by disrupting specific junctional adhesion molecules.
Highlights
Specialty section: This article was submitted to Oral Infections and Microbes, a section of the journal Frontiers in Oral Health
To assess the molecular basis of gingival epithelial barrier dysfunction associated with P. gingivalis, we newly developed a three-dimensional multilayered tissue model of gingival epithelium with gene manipulation
We confirmed that the immature forms of junctional adhesion molecule 1 (JAM1) and coxsackievirus and adenovirus receptor (CXADR) possessed a signal peptide and were localized in the endoplasmic reticulum [11, 12]
Summary
Epithelial cells are located on the front line of infection defense, and function as a physical barrier against pathogenic bacteria and their products. Human gingival epithelial cells have been reported to express tight-junction associated proteins, such as claudin, occludin, junctional adhesion molecule 1 (JAM1), and zonula occludens-1 [1], among which JAM1, an immunoglobulin superfamily protein, reportedly localizes in mucosal epithelium of numerous organs [2]. Periodontitis is basically an infectious disease that causes destruction of periodontal tissues by interactions between periodontal pathogens and host cells [3]. Since gingival epithelial cells are the first to face periodontal pathogens, gingival epithelial tissues are potentially involved in the pathogenesis and progress of periodontitis. Periodontal diseases are multispecies infections involving pathogenic communities in which P. gingivalis can increase the pathogenicity of the entire multispecies periodontal community [3]
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