TY - JOUR
T1 - In vitro modeling of host-parasite interactions
T2 - The 'subgingival' biofilm challenge of primary human epithelial cells
AU - Guggenheim, Bernhard
AU - Gmür, Rudolf
AU - Galicia, Johnah C.
AU - Stathopoulou, Panagiota G.
AU - Benakanakere, Manjunatha R.
AU - Meier, André
AU - Thurnheer, Thomas
AU - Kinane, Denis F.
N1 - Funding Information:
We thank Dr. Chris Wyss for the preparation of T. forsythia cultures and helpful discussions. We thank Helga Lüthi-Schaller for excellent assistance with FISH and IF, and Steve Reese for performing the TEM. This work was in part supported by the University of Zürich and United States Public Health Service, National Institutes of Health, NIDCR grant DE017384 to DFK.
PY - 2009
Y1 - 2009
N2 - Background. Microbial biofilms are known to cause an increasing number of chronic inflammatory and infectious conditions. A classical example is chronic periodontal disease, a condition initiated by the subgingival dental plaque biofilm on gingival epithelial tissues. We describe here a new model that permits the examination of interactions between the bacterial biofilm and host cells in general. We use primary human gingival epithelial cells (HGEC) and an in vitro grown biofilm, comprising nine frequently studied and representative subgingival plaque bacteria. Results. We describe the growth of a mature 'subgingival' in vitro biofilm, its composition during development, its ability to adapt to aerobic conditions and how we expose in vitro a HGEC monolayer to this biofilm. Challenging the host derived HGEC with the biofilm invoked apoptosis in the epithelial cells, triggered release of pro-inflammatory cytokines and in parallel induced rapid degradation of the cytokines by biofilm-generated enzymes. Conclusion. We developed an experimental in vitro model to study processes taking place in the gingival crevice during the initiation of inflammation. The new model takes into account that the microbial challenge derives from a biofilm community and not from planktonically cultured bacterial strains. It will facilitate easily the introduction of additional host cells such as neutrophils for future biofilm:host cell challenge studies. Our methodology may generate particular interest, as it should be widely applicable to other biofilm-related chronic inflammatory diseases.
AB - Background. Microbial biofilms are known to cause an increasing number of chronic inflammatory and infectious conditions. A classical example is chronic periodontal disease, a condition initiated by the subgingival dental plaque biofilm on gingival epithelial tissues. We describe here a new model that permits the examination of interactions between the bacterial biofilm and host cells in general. We use primary human gingival epithelial cells (HGEC) and an in vitro grown biofilm, comprising nine frequently studied and representative subgingival plaque bacteria. Results. We describe the growth of a mature 'subgingival' in vitro biofilm, its composition during development, its ability to adapt to aerobic conditions and how we expose in vitro a HGEC monolayer to this biofilm. Challenging the host derived HGEC with the biofilm invoked apoptosis in the epithelial cells, triggered release of pro-inflammatory cytokines and in parallel induced rapid degradation of the cytokines by biofilm-generated enzymes. Conclusion. We developed an experimental in vitro model to study processes taking place in the gingival crevice during the initiation of inflammation. The new model takes into account that the microbial challenge derives from a biofilm community and not from planktonically cultured bacterial strains. It will facilitate easily the introduction of additional host cells such as neutrophils for future biofilm:host cell challenge studies. Our methodology may generate particular interest, as it should be widely applicable to other biofilm-related chronic inflammatory diseases.
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U2 - 10.1186/1471-2180-9-280
DO - 10.1186/1471-2180-9-280
M3 - Article
C2 - 20043840
AN - SCOPUS:77149132131
SN - 1471-2180
VL - 9
JO - BMC Microbiology
JF - BMC Microbiology
M1 - 280
ER -