Abstract
Periodontitis is a global health problem and the 6th most common infectious disease worldwide. Porphyromonas gingivalis is considered a keystone pathogen in the disease and is capable of elevating the virulence potential of the periodontal microbial community. Strategies that interfere with P. gingivalis colonization and expression of virulence factor are therefore attractive approaches for preventing and treating periodontitis. We have previously reported that an 11-mer peptide (SAPP) derived from Streptococcus cristatus arginine deiminase (ArcA) was able to repress the expression and production of several well-known P. gingivalis virulence factors including fimbrial proteins and gingipains. Herein we expand and develop these studies to ascertain the impact of this peptide on phenotypic properties of P. gingivalis related to virulence potential. We found that growth rate was not altered by exposure of P. gingivalis to SAPP, while monospecies and heterotypic biofilm formation, and invasion of oral epithelial cells were inhibited. Additionally, SAPP was able to impinge the ability of P. gingivalis to dysregulate innate immunity by repressing gingipain-associated degradation of interleukin-8 (IL8). Hence, SAPP has characteristics that could be exploited for the manipulation of P. gingivalis levels in oral communities and preventing realization of virulence potential.
Highlights
Dental plaque is a complex multispecies biofilm that is a direct precursor of periodontal diseases
In an in vitro study, we demonstrated that S. cristatus ArcA significantly inhibited biofilm formation by P. gingivalis[25] and using a mouse model, we found that S. cristatus ArcA can interfere with the colonization and pathogenesis of P. gingivalis[26]
The effect of W83 on monotypic biofilm formation was tested with the bacterial cells grown with 24 or 48 μM SAPP
Summary
Dental plaque is a complex multispecies biofilm that is a direct precursor of periodontal diseases. Several specific oral bacteria are associated with periodontitis, a new model of pathogenesis proposes that polymicrobial synergy among organisms in periodontal microbial communities initiates dysbiotic and destructive immune responses[11]. In this model, transition from a commensal to a pathogenic microbial community requires the colonization of keystone pathogens such as P. gingivalis. P. gingivalis interspecies interactions subsequently elevate the virulence of the entire microbial community[14,15,16,17] This phenomenon is evident in murine models, in which low levels of P. gingivalis can initiate alveolar bone loss, but only in the context of a microbial community[14]. Our findings demonstrate the potential of SAPP as a lead compound for the development of therapeutic agents designed to inhibit P. gingivalis colonization and pathogenicity
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