AI Article Synopsis

  • This study examined how a specific bacteria impacts periodontal cells, focusing on its invasion and effects on cell growth and cycle phases.
  • Researchers used a model with human periodontal ligament fibroblasts and different concentrations of the bacteria to analyze cell proliferation and cycle changes.
  • Results showed that the bacteria inhibited cell growth and caused G2 phase arrest, with more significant effects at higher concentrations, indicating a complex interaction that disrupts normal cell cycle regulation.

Article Abstract

Purpose: Several studies have shown that the oral cavity is a secondary location for colonization and that is associated with the severity of periodontitis. This study investigated whether had an effect on the periodontium. We established an invasion model of a standard strain of in human periodontal ligament fibroblasts (hPDLFs), and evaluated the effects of on cell proliferation and cell cycle progression.

Methods: Different concentrations of were used to infect hPDLFs, with 6 hours of co-culture. The multiplicity of infection in the low- and high-concentration groups was 10:1 and 100:1, respectively. The Cell Counting Kit-8 method and Ki-67 immunofluorescence were used to detect cell proliferation. Flow cytometry, quantitative real-time polymerase chain reaction, and western blots were used to detect cell cycle progression. In the high-concentration group, the invasion of was observed by transmission electron microscopy.

Results: It was found that invaded the fibroblasts, with cytoplasmic localization. Analyses of cell proliferation and flow cytometry showed that inhibited the proliferation of periodontal fibroblasts by causing G2 phase arrest. The inhibition of proliferation and G2 phase arrest were more obvious in the high-concentration group. In the low-concentration group, the G2 phase regulatory factors cyclin dependent kinase 1 (CDK1) and cell division cycle 25C (Cdc25C) were upregulated, while cyclin B1 was inhibited. However, in the high-concentration group, cyclin B1 was upregulated and CDK1 was inhibited. Furthermore, the deactivated states of tyrosine phosphorylation of CDK1 (CDK1-Y15) and serine phosphorylation of Cdc25C (Cdc25C-S216) were upregulated after infection.

Conclusions: In our model, inhibited the proliferation of hPDLFs and exerted an invasive effect, causing G2 phase arrest via the Cdc25C/CDK1/cyclin B1 signaling cascade. Its inhibitory effect on proliferation was stronger in the high-concentration group.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6599755PMC
http://dx.doi.org/10.5051/jpis.2019.49.3.138DOI Listing

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