Gingival and periodontal ligament fibroblasts differ in their inflammatory response to viable Porphyromonas gingivalis.
OBJECTIVE
Porphyromonas gingivalis is an oral pathogen strongly associated with destruction of the tooth-supporting tissues in human periodontitis. Gingival fibroblasts (GF) and periodontal ligament fibroblasts (PDLF) are functionally different cell types in the periodontium that can participate in the host immune response in periodontitis. This study aimed to investigate the effects of viable P. gingivalis on the expression of genes associated with inflammation and bone degradation by these fibroblast subsets.


METHODS
Primary human GF and PDLF from six healthy donors were challenged in vitro with viable P. gingivalis W83 for 6 h. Gene expression of inflammatory cytokines in GF and PDLF was analyzed using real-time PCR, and protein expression was analyzed using ELISA.


RESULTS
Viable P. gingivalis induced a strong in vitro inflammatory response in both GF and PDLF. We found increased gene expression of interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor-alpha, monocyte chemotactic protein-1 and regulated upon activation, normal T-cell expressed and secreted (RANTES). Macrophage colony-stimulating factor was induced and the expression of osteoprotegerin was decreased in GF, but not in PDLF. In nonchallenged cells, a higher level of expression of IL-6 was observed in GF than in PDLF. Between individual donors there was large heterogeneity in responsiveness to P. gingivalis. Also, in each individual, either GF or PDLF was more responsive to P. gingivalis.


CONCLUSIONS
Considerable heterogeneity in responsiveness to P. gingivalis exists both between GF and PDLF and between individuals, which may be crucial determinants for the susceptibility to develop periodontitis.
Scheres
N
N
Departments of Oral Microbiology, Oral Cell Biology and Periodontology, Academic Centre for Dentistry Amsterdam, University of Amsterdam and VU University Amsterdam, Research Institute MOVE, the Netherlands.
Laine
M L
ML
de Vries
T J
TJ
Everts
V
V
van Winkelhoff
A J
AJ
D000293:Adolescent; D000328:Adult; D000469:Alkaline Phosphatase / Q000032:analysis; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000032:analysis; D018946:Chemokine CCL5 / Q000032:analysis; D016207:Cytokines / Q000032:analysis; D005260:Female; D005347:Fibroblasts / Q000276:immunology / Q000382:microbiology*; D005881:Gingiva / Q000166:cytology* / Q000276:immunology / Q000382:microbiology; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D008213:Lymphocyte Activation / Q000276:immunology; D016173:Macrophage Colony-Stimulating Factor / Q000032:analysis; D008297:Male; D053244:Osteoprotegerin / Q000032:analysis; D010513:Periodontal Ligament / Q000166:cytology* / Q000276:immunology / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D055815:Young Adult
D018932:Chemokine CCL2; D018946:Chemokine CCL5; D016207:Cytokines; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D053244:Osteoprotegerin; D014409:Tumor Necrosis Factor-alpha; D016173:Macrophage Colony-Stimulating Factor; D000469:Alkaline Phosphatase