Binding of Streptococcus gordonii to oral epithelial monolayers increases paracellular barrier function.

The junctional epithelium comprising the gingival attachment to the tooth acts as a barrier against pathogenic subgingival plaque microbes and their products. There is evidence that pathogenic Porphyromonas gingivalis has the potential to disrupt epithelial integrity, contributing to breakdown of the junctional epithelium characteristic of the immunopathological response of chronic periodontitis. The present study investigated the capacity of the oral commensal Streptococcus gordonii to increase epithelial barrier function to support epithelial integrity of healthy tissue. Oral epithelial barrier function was measured by permeability assay. Changes in expression of tight junction components were monitored by quantitative real-time RT-PCR and Western blot in an oral epithelial cell culture model following binding by S. gordonii strain FSS2. The data showed increased expression of genes encoding the tight junction components ZO-1, ZO-2, JAM-A, and occludin at a ratio of 100 bacterial colony forming units per epithelial cell. This was associated with increased expression at the protein level of ZO-1, ZO-2 and JAM-A. Reduction of permeability to fluorochrome-labelled dextran accompanied these changes. The data support the hypothesis that (some) commensal bacteria have a beneficial effect on oral epithelium.