Global Transcriptional Analysis Reveals Upregulation of NF-${\kappa}B$-responsive and Interferon-stimulated Genes in Monocytes by Treponema lecithinolyticum Major Surface Protein

  • Lee, Sung-Hoon (Department of Oral Microbiology and Immunology, School of Dentistry, Seoul National University) ;
  • Lee, Hae-Ri (Department of Oral Microbiology and Immunology, School of Dentistry, Seoul National University) ;
  • Jun, Hye-Kyoung (Department of Oral Microbiology and Immunology, School of Dentistry, Seoul National University) ;
  • Choi, Bong-Kyu (Department of Oral Microbiology and Immunology, School of Dentistry, Seoul National University)
  • Received : 2011.04.29
  • Accepted : 2011.06.10
  • Published : 2011.06.30

Abstract

MspTL is the major surface protein of Treponema lecithinolyticum associated with periodontitis and endodontic infections. Our recent investigation revealed that MspTL induces proinflammatory cytokines and intercellular adhesion molecule 1 in THP-1 cells and periodontal ligament cells. In this study we conducted oligonucleotide microarray analysis to investigate the global transcriptional regulation in THP-1 cells stimulated with purified recombinant MspTL. MspTL upregulated the expression of 90 genes in THP-1 cells at least four fold, and the functions of these genes were categorized into adhesion, apoptosis/antiapoptosis, cell cycle/growth/differentiation, chemotaxis, cytoskeleton organization, immune response, molecular metabolism, proteolysis, signaling, and transcription. The majority of the modified genes are known to be NF-${\kappa}B$-responsive and interferon-stimulated genes (ISGs). The expression of 12 selected genes was confirmed by real-time RT-PCR. Because prostaglandin $E_2(PGE_2)$ is an important inflammatory mediator and Cox-2 was found to be induced by MspTL in the microarray analysis, we determined the level of $PGE_2$ in the culture supernatants of MspTL-treated cells and found that MspTL significantly increased $PGE_2$. Our results provide insight into the gene regulation of host cells in response to MspTL, and may contribute to the understanding of the molecular mechanism in periodontitis.

Keywords

References

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