Abstract
BackgroundControl of intercellular penetration of microbial products is critical for the barrier function of oral epithelia. We demonstrated that CD24 is selectively and strongly expressed in the cells of the epithelial attachment to the tooth and the epithelial lining of the diseased periodontal pocket and studies in vitro showed that CD24 regulated expression of the epithelial intercellular adhesion protein E-cadherin.ResultsIn the present study, the barrier function of oral epithelial cell monolayers to low molecular weight dextran was assayed as a model for the normal physiological function of the epithelial attachment to limit ingress of microbial products from oral microbial biofilms. Paracellular transfer of low molecular weight dextran across monolayers of oral epithelial cells was specifically decreased following incubation with anti-CD24 peptide antibody whereas passage of dextran across the monolayer was increased following silencing of mRNA for CD24. Changes in barrier function were related to the selective regulation of the genes encoding zonula occludens-1, zonula occludens-2 and occludin, proteins implicated in tight junctions. More particularly, enhanced barrier function was related to relocation of these proteins to the cell periphery, compatible with tight junctions.ConclusionCD24 has the constitutive function of maintaining expression of selected genes encoding tight junction components associated with a marginal barrier function of epithelial monolayers. Activation by binding of an external ligand to CD24 enhances this expression but is also effective in re-deployment of tight junction proteins that is aligned with enhanced intercellular barrier function. These results establish the potential of CD24 to act as a potent regulator of the intercellular barrier function of epithelia in response to local microbial ecology.
Highlights
Control of intercellular penetration of microbial products is critical for the barrier function of oral epithelia
This antigen is recognized by auto-reactive serum antibodies in patients with chronic periodontal disease [3] and increased titres of antibodies reactive with CD24 peptide correlated with more favourable diagnosis, suggesting a protective effect [3]
Anti-CD24 peptide antibody reduces passage of dextran across the epithelial monolayers Monolayers were cultured to confluence on membranes within diffusion chambers as described in Methods
Summary
Control of intercellular penetration of microbial products is critical for the barrier function of oral epithelia. Intra- and inter-cellular signaling occurring through interaction between CD24 and L1 could be modulated by lectin-like molecules such as the sialic acid binding protein Hsa from Streptococcus gordonii, an early coloniser in bacterial plaque [8], or by antibodies that recognize CD24 [3]. These ligands for CD24 have potential to either activate signaling through CD24 or perturb signals mediated by constitutive interaction between CD24 and L1
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