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* Department of Periodontology, Faculty of Dentistry,
Research Unit for Periodontal Disease, Immunology Laboratory, Faculty of Dentistry, and
Department of Oral Maxillofacial Surgery, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand; and
Department of Immunology and Medicine, United States Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand
Human gingival fibroblasts (HGFs), a predominant cell type in tooth-supporting structure, are presently recognized for their active role in the innate immune response. They produce a variety of inflammatory cytokines in response to microbial components such as LPS from the key periodontal pathogen, Porphyromonas gingivalis. In this study, we demonstrated that HGFs expressed mRNA of TLRs 1, 2, 3, 4, 5, 6, and 9, but not TLRs 7, 8, and 10. Stimulation of HGFs with highly purified TLR2 ligand (P. gingivalis LPS), TLR3 ligand (poly(I:C)), TLR4 ligand (Escherichia coli LPS), and TLR5 ligand (Salmonella typhimurium flagellin) led to expression of IL-8 and IDO. A potent TLR 9 ligand, CpG oligodeoxynucleotide 2006 had no effect, although HGFs showed a detectable TLR9 mRNA expression. No significant enhancement on IL-8 or IDO expression was observed when HGFs were stimulated with various combinations of TLR ligands. Surprisingly, the TLR9 ligand CpG oligodeoxynucleotide 2006 was able to specifically inhibit poly(I:C)-induced IL-8 and IDO expression. TNF-
enhanced TLR ligand-induced IL-8 production in HGFs, whereas IFN-
enhanced TLR ligand-induced IDO expression. HGF production of IDO in response to P. gingivalis LPS, IFN-, or the two in combination inhibited T cell proliferation in MLRs. The observed T cell inhibition could be reversed by addition of either 1-methyl-DL-tryptophan or L-tryptophan. Our results suggest an important role of HGFs not only in orchestrating the innate immune response, but also in dampening potentially harmful hyperactive inflammation in periodontal tissue.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by the Thailand Research Fund (BRG-4980006) and Ratchapisek Endowment.
2 Address correspondence and reprint requests to Dr. Rangsini Mahanonda, Department of Periodontology, Faculty of Dentistry, Chulalongkorn University, Henry Dunant Road, Bangkok, Thailand. E-mail address: mrangsin{at}chula.ac.th
3 Abbreviations used in this paper: HGF, human gingival fibroblast; PAMP, pathogen-associated molecular patterns; ODN, oligodeoxynucleotide.
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