Laurate Butyl Glucoside Enhances Oral Innate Immunity Without Increasing Inflammation

Objectives: Oral epithelium is both involved in host defence and in the pathogenesis of inflammatory disorders. In humans, it plays a critical role in innate immune response by producing antimicrobial peptides, with immuno-modulatory and microbicidal properties, such as natural antibiotics. Among them, beta-defensins are inducible, triggered by injury or inflammation of the gingival epithelium. We focused on active principles that could promote innate immunity without enhancing inflammation. We used several in vitro cellular and tissue models to study the effect of LaurateButylGlucoside (LBG) on the regulation of HBD-2 and HBD-3 expression. Methods: In vitro, reconstructed or native gingival epithelium and normal gingival keratinocytes (NGK) were treated with pro-inflammatory cytokines, microbial components and increasing concentrations of LBG. The expression of HBD-2 and HBD-3 were studied by immuno-histochemical analysis and their respective messenger RNA levels were assayed with quantitative, RT-PCR. Inflammatory response was investigated by quantifying the level of the secreted IL–8 by ELISA. Results: Firstly, we demonstrated that the models we designed, were functional for the modulation of HBD expression in vitro. Secondly, after a 3 day-differentiation stage, NGK were incubated with positive controls and LBG. m-RNA analysis showed that LBG induced HBD-2 and HBD-3 in a dose dependant manner. Meanwhile, the level of secreted IL-8 remained stable. Moreover, we demonstrated that LBG significantly stimulated endogenous HBD-2 and HBD-3 mRNA in reconstructed or native epithelia. Immuno-histochemistry showed that both peptides were rapidly increased in the upper layers of the stratified epithelia. Conclusion: Together these data demonstrated that LBG could be considered as a regulator of oral innate immunity without promoting inflammation. Thereby, we supposed that it could prevent the ecological balance to be disturbed and the subsequent colonization by gram negative microflora becoming pathogens.