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Review
. 2010 Feb;52(1):68-83.
doi: 10.1111/j.1600-0757.2009.00323.x.

Bacterial invasion of epithelial cells and spreading in periodontal tissue

Gena D Tribble, Richard J Lamont
Review

Bacterial invasion of epithelial cells and spreading in periodontal tissue

Gena D Tribble et al. Periodontol 2000. 2010 Feb.
No abstract available

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Invasion of human epithelial cells with Porphyromonas gingivalis. Confocal image of gingival epithelial cells [stained with TRITC-phalloidin (red)] infected with P. gingivalis [stained with FITC (green)]. The image was analyzed using Imaris version 5.0.1 software. A Z-stack of the x–y sections was converted to composite images using the iso surface and spot detection functions of the surpass option. The section view in the x and y axes was created using the clipping function. The image was generated by Masae Kuboniwa, Osaka University, Japan.
Fig. 2
Fig. 2
Model of interactions between Porphyromonas gingivalis and gingival epithelial cells that are associated with internalization. Proximity to gingival epithelial cells induces P. gingivalis to secrete proteins such as the SerB serine phosphatase. SerB enters gingival epithelial cells where it dephosphorylates target proteins, including mitogen-activated protein kinase family members, which in turn prevent NF-κB activation. SerB activity culminates in a reduction of interleukin-8 production and in the remodeling of microfilament and microtubule cytoskeletal architecture. Adhesion of P. gingivalis is mediated by the long (FimA) fimbriae that engage integrins and induce the formation of focal adhesin complexes and integrin-dependent signaling. Calcium ions (Ca2+) are released from intracellular stores, a signaling event that also funnels through the cytoskeletal structure, and the cytoskeletal re-arrangements allow P. gingivalis to enter the host cell. P. gingivalis cells rapidly locate in the perinuclear area where they replicate and utilize microfilaments to spread to adjacent gingival epithelial cells. CM, cytoplasmic membrane; IL-8, interleukin-8; IκB, inhibitor of κB; MAP, mitogen-activated protein kinase; MF, micro-filament; MT, microtubule; NF-κB, nuclear factor-κB; P, phosphate.
Fig. 3
Fig. 3
Summary of major apoptotic pathways modulated by Porphyromonas gingivalis in gingival epithelial cells to suppress apoptotic cell death. Jak1; P; PI3K; PIP3; Stat3.
Fig. 4
Fig. 4
Porphyromonas gingivalis impacts cell cycle control in gingival epithelial cells. Schematic representation of cell cycle pathways modulated by P. gingivalis infection. The pointed arrow indicates molecular interactions resulting in activation; the flat arrow indicates molecular interactions resulting in inhibition. Reprinted with permission from Microbes and Infection 2008, 10:122-128, Copyright Elsevier (70).
See this image and copyright information in PMC

References

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