Transcriptional profiling of human gingival fibroblasts in response to multi-species in vitro subgingival biofilms.
Periodontitis is an infectious inflammatory disease that destroys the tooth-supporting tissues. It is initiated by complex subgingival biofilms, triggering an inflammatory response by the juxtaposed gingival tissue. The range of transcriptional events initiated in the gingiva following biofilm challenge is not fully elucidated. By employing gene microarray technology, this study aimed to characterize the overall transcriptional changes (more than two-fold regulation) of cultured human gingival fibroblasts in response to a 10-species in vitro subgingival biofilm model (BF), over a challenge period of 6 h. The relative involvement of the three 'red complex' species in these transcriptional events was evaluated by omitting these species from the biofilm composition (BF-RC). When compared with the unchallenged control, challenge with BF and BF-RC differentially regulated 386 and 428 genes, respectively, with an overlap of 52-75%. Interestingly, the expression of only three genes was significantly different between the BF and BF-RC challenged groups. There was also a strong overlap of the affected signalling pathways and gene ontology processes. These signalling pathways involved primarily the immune response, and included toll-like receptors, interleukin-1, interleukin-17 and heat-shock proteins 60 and 70. In conclusion, subgingival biofilms elicited a large number of transcriptional changes in gingival fibroblasts, while the presence of the 'red complex' in the biofilm did not yield any substantial differences. These findings show a uniform 'non-specific' transcriptional response of host cells to subgingival biofilms, and denote that redundancies may exist in the virulence properties of individual bacterial species within a polymicrobial biofilm community.
Oral Microbiology and Immunology, Institute of Oral Biology, Centre of Dental Medicine, University of Zürich, Zürich, Switzerland.
G N
GN
Belibasakis
K
K
Bao
N
N
Bostanci
D018441:Biofilms / Q000254:growth & development*; D002478:Cells, Cultured; D018834:Chaperonin 60 / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism* / Q000382:microbiology*; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D005881:Gingiva / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology*; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D010518:Periodontitis / Q000382:microbiology; D051193:Toll-Like Receptors / Q000378:metabolism / Q000502:physiology
D018834:Chaperonin 60; D018840:HSP70 Heat-Shock Proteins; D007375:Interleukin-1; D020381:Interleukin-17; D053583:Interleukin-1beta; D051193:Toll-Like Receptors
gene microarray; gingival fibroblasts; periodontal disease; red complex; subgingival biofilm; transcriptional profiling