Human gingival fibroblasts release high-mobility group box-1 protein through active and passive pathways

  1. K. Feghali1,2,
  2. K. Iwasaki1,
  3. K. Tanaka1,
  4. M. Komaki3,
  5. M. Machigashira4,
  6. I. Ishikawa5,
  7. Y. Izumi1,2

Article first published online: 15 JUN 2009

DOI: 10.1111/j.1399-302X.2009.00508.x

Issue

Oral Microbiology and Immunology

Oral Microbiology and Immunology

Volume 24, Issue 4, pages 292–298, August 2009

Additional Information

How to Cite

Feghali, K., Iwasaki, K., Tanaka, K., Komaki, M., Machigashira, M., Ishikawa, I. and Izumi, Y. (2009), Human gingival fibroblasts release high-mobility group box-1 protein through active and passive pathways. Oral Microbiology and Immunology, 24: 292–298. doi: 10.1111/j.1399-302X.2009.00508.x

Author Information

  1. 1

    Section of Periodontology, Department of Hard Tissue Engineering, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan

  2. 2

    Global Centre of Excellence (GCOE) Program, International Research Center for Molecular Science in Tooth and Bone Diseases, Tokyo Medical and Dental University, Tokyo, Japan

  3. 3

    Department of Nanomedicine(DNP), Tokyo Medical and Dental University, Tokyo, Japan

  4. 4

    Department of Periodontology, Kagoshima University, Graduate School of Medical and Dental Sciences, Kagoshima, Japan

  5. 5

    Institute of Advanced Biomedical Engineering and Science, Tokyo Women’s Medical University, Tokyo, Japan

*Kengo Iwasaki, Section of Periodontology, Department of Hard Tissue Engineering, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8549, Japan Tel.: +81 3 5803 5488; fax: +81 3 5803 0196; e-mail: k-iwasaki.peri@tmd.ac.jp

Publication History

  1. Issue published online: 15 JUN 2009
  2. Article first published online: 15 JUN 2009
  3. Accepted for publication December 22, 2008

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Keywords:

  • apoptosis;
  • high-mobility group box 1;
  • human gingival fibroblasts;
  • lipopolysaccharides;
  • necrosis

Introduction:  The nuclear protein high-mobility group box-1 (HMGB1) acts as a late mediator of inflammation when secreted in the extracellular milieu. In this study, we examined the effect of lipopolysaccharides from periodontal pathogens and apoptotic and necrotic cell death on HMGB1 production in human gingival fibroblasts (HGF).

Methods:  HGF from healthy periodontal tissue were cultured and stimulated with lipopolysaccharides (LPS) from Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Escherichia coli. We also initiated apoptotic and necrotic cell deaths in HGF. The HMGB1 released in the supernatants from stimulated or dying cells was measured. Immunocytochemical staining against HMGB1 was performed in LPS-stimulated HGF.

Results:  A significantly higher amount of HMGB1 was detected from necrotic and apoptotic HGF. LPS from A. actinomycetemcomitans, P. gingivalis, and E. coli significantly induced the production of HMGB1 in a time-dependent manner. After 6 h of LPS stimulation, HMGB1 was present in the cytoplasm of cells whereas its location was mainly nuclear after 24 h.

Conclusions:  LPS from two major periodontal pathogens, A. actinomycetemcomitans and P. gingivalis, induced HMGB1 secretion from HGF. Apoptotic and necrotic cell deaths resulted in the enhancement of HMGB1. Our results suggest that HGF can be a source of HMGB1 by both active secretion and passive release, and that HMGB1 from HGF may contribute to periodontal tissue destruction.

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