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Toll-like Receptor3-mediated Induction of Chemokines in Salivary Epithelial Cells

  • Li, Jingchao (Department of Physiology, School of Dentistry, Seoul National University and Dental Research Institute) ;
  • Jeong, Mi-Young (Department of Physiology, School of Dentistry, Seoul National University and Dental Research Institute) ;
  • Bae, Ji-Hyun (Department of Physiology, School of Dentistry, Seoul National University and Dental Research Institute) ;
  • Shin, Yong-Hwan (Department of Physiology, School of Dentistry, Seoul National University and Dental Research Institute) ;
  • Jin, Meihong (Department of Physiology, School of Dentistry, Seoul National University and Dental Research Institute) ;
  • Hang, Sung-Min (Department of Physiology, School of Dentistry, Seoul National University and Dental Research Institute) ;
  • Lee, Jeong-Chai (R&D Center of Medi-Future) ;
  • Lee, Sung-Joong (Department of Physiology, School of Dentistry, Seoul National University and Dental Research Institute) ;
  • Park, Kyung-Pyo (Department of Physiology, School of Dentistry, Seoul National University and Dental Research Institute)
  • Received : 2010.08.02
  • Accepted : 2010.08.11
  • Published : 2010.08.30

Abstract

Toll-like receptors (TLRs) functionally expressed in salivary epithelial cells, but their roles remain elusive. Among TLRs family, TLR3 is activated by dsRNA, a byproduct of viral infection. The aim of this study was to investigate the role of TLR3 in the inflammatory immune responses using HSG cells. Reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR and ELISA were performed to identify expression of TLRs and TLR3-mediated chemokine inductions. The chemotaxis assay of activated T lymphocytes was also performed. Treatment of HSG cells with polyinosinic: polycytidylic acid (poly(I:C)) significantly increased interferon-$\gamma$-inducible protein 10 (IP-10), interferoninducible T-cell $\alpha$ chemoattractant (I-TAC), and regulated on activation, normal T-cells expressed and secreted (RANTES) gene expressions in a concentration-dependent manner. Anti-TLR3 antibody blocked the increases of IP-10 and I-TAC genes. Poly(I:C)-induced increases of IP-10 and I-TAC were also confirmed at protein levels from cell lysates, but their release into extracellular medium was detected only in IP-10. We found that the culture media from HSG cells stimulated with poly(I:C) significantly increases T lymphocyte migration. Our results suggest that TLR3 plays an important role in chemokine induction, particularly IP-10, in salivary epithelial cells.

Keywords

References

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