The capsule of Porphyromonas gingivalis reduces the immune response of human gingival fibroblasts.
BACKGROUND
Periodontitis 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.


RESULTS
To 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-1beta, 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-1beta to five times higher for IL-8.


CONCLUSIONS
These 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.
Brunner
Jorg
J
Department of Oral Microbiology, Academic Centre for Dentistry Amsterdam, Universiteit van Amsterdam and Vrije Universiteit, Amsterdam, The Netherlands. w.crielaard@acta.nl
Scheres
Nina
N
El Idrissi
Nawal B
NB
Deng
Dong M
DM
Laine
Marja L
ML
van Winkelhoff
Arie J
AJ
Crielaard
Wim
W
D016667:Bacterial Capsules / Q000235:genetics / Q000276:immunology*; D002478:Cells, Cultured; D005347:Fibroblasts / Q000276:immunology*; D055786:Gene Knockout Techniques; D005881:Gingiva / Q000276:immunology* / Q000382:microbiology; D054884:Host-Pathogen Interactions; D006801:Humans; D053583:Interleukin-1beta / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D016209:Interleukin-8 / Q000276:immunology; D016254:Mutagenesis, Insertional; D010518:Periodontitis / Q000276:immunology; D016966:Porphyromonas gingivalis / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity*; D014774:Virulence
D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8