Induction of Signal Transduction Pathway Genes in Dendritic Cells by Lipopolysaccharides from Porphyromonas gingivalis and Escherichia coli

  • Jin, Ho-Kyeong (Department of Oral Microbiology, School of Dentistry, Pusan National University) ;
  • Lee, Young-Hwa (Department of Oral Microbiology, School of Dentistry, Pusan National University) ;
  • Jeong, So-Yeon (Department of Oral Microbiology, School of Dentistry, Pusan National University) ;
  • Na, Hee-Sam (Department of Oral Microbiology, School of Dentistry, Pusan National University) ;
  • Park, Hae-Ryoun (Department of Oral Pathology, School of Dentistry, Pusan National University) ;
  • Chung, Jin (Department of Oral Microbiology, School of Dentistry, Pusan National University)
  • Received : 2010.09.01
  • Accepted : 2010.09.24
  • Published : 2010.09.30

Abstract

Porphyromonas (P.) gingivalis lipopolysaccharide (Pg LPS) is the major pathogenic component of periodontal disease. In this study, we have attempted to determine the expression profiles of the signal transduction pathway genes induced by Pg LPS in comparison with Escherichia (E.) coli LPS (Ec LPS). DC2.4 cells were treated for two hours with $1\;{\mu}g/ml$ of Pg LPS or $0.5\;{\mu}g/ml$ of Ec LPS. The total RNA from these cells was then isolated and reverse-transcribed. Gene expression profiles were then analyzed with a signal transduction pathway finder GEArray Q series kit and significant changes in expression were confirmed by real-time PCR. The microarray results indicated that several genes, including Tnfrsf10b, Vcam1, Scyb9, Trim25, Klk6, and Stra6 were upregulated in the DC2.4 cells in response to Pg LPS treatment, but were downregulated or unaffected by Ec LPS. Realtime PCR revealed that the expression of Trim25, Scyb9 and Tnfrsf10b was increased over the untreated control. Notably, Trim25 and Tnfrsf10b were more strongly induced by Pg LPS than by Ec LPS. These results provide greater insight into the signal transduction pathways that are altered by P. gingivalis LPS.

Keywords

References

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