Abstract
BackgroundPeriodontitis is a bacterial infection of the periodontal tissues. The Gram-negative anaerobic bacterium Porphyromonas gingivalis is considered a major causative agent. One of the virulence factors of P. gingivalis is capsular polysaccharide (CPS). Non-encapsulated strains have been shown to be less virulent in mouse models than encapsulated strains.ResultsTo examine the role of the CPS in host-pathogen interactions we constructed an insertional isogenic P. gingivalis knockout in the epimerase-coding gene epsC that is located at the end of the CPS biosynthesis locus. This mutant was subsequently shown to be non-encapsulated. K1 capsule biosynthesis could be restored by in trans expression of an intact epsC gene. We used the epsC mutant, the W83 wild type strain and the complemented mutant to challenge human gingival fibroblasts to examine the immune response by quantification of IL-1β, IL-6 and IL-8 transcription levels. For each of the cytokines significantly higher expression levels were found when fibroblasts were challenged with the epsC mutant compared to those challenged with the W83 wild type, ranging from two times higher for IL-1β to five times higher for IL-8.ConclusionsThese experiments provide the first evidence that P. gingivalis CPS acts as an interface between the pathogen and the host that may reduce the host's pro-inflammatory immune response. The higher virulence of encapsulated strains may be caused by this phenomenon which enables the bacteria to evade the immune system.
Highlights
Periodontitis is a bacterial infection of the periodontal tissues
It has been reported that the capsular polysaccharide (CPS) of K1 comprises of mannuronic acid (ManA), glucuronic acid (GlcA), galacturonic acid (GalA), galactose and N-acetylglucosamine (GlcNAc), but the CPS structure has not been solved [12]
This study provides the first direct evidence that P. gingivalis CPS reduces the host immune response, thereby potentially enabling evasion of the immune system to sustain successful long-term infection
Summary
Periodontitis is a bacterial infection of the periodontal tissues. The Gram-negative anaerobic bacterium Porphyromonas gingivalis is considered a major causative agent. Among the variety of virulence factors that have been described for P. gingivalis, CPS has shown to be a major factor in experimental infections. Studies in a mouse infection model have revealed that encapsulated P. gingivalis strains are more virulent than non-encapsulated. CPS of all serotypes has been tested for induction of immunological responses in macrophages and it has been revealed that the CPS of K1 serotype strains induces higher chemokine expression in murine peritoneal macrophages than the other serotypes [11]. These data suggest that the K1 CPS plays an important role in host-pathogen interaction. It has been reported that the CPS of K1 (strain W50) comprises of mannuronic acid (ManA), glucuronic acid (GlcA), galacturonic acid (GalA), galactose and N-acetylglucosamine (GlcNAc), but the CPS structure has not been solved [12]
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