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Infection and Immunity, May 2008, p. 2080-2089, Vol. 76, No. 5
0019-9567/08/$08.00+0     doi:10.1128/IAI.01428-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Interleukin-1β Modulates Proinflammatory Cytokine Production in Human Epithelial Cells{triangledown}

Mehmet A. Eskan, Manjunatha R. Benakanakere, Beate G. Rose, Ping Zhang, Jiawei Zhao, Panagiota Stathopoulou, Daisuke Fujioka, and Denis F. Kinane*

Oral Health and Systemic Disease, Department of Periodontics, Endodontics and Dental Hygiene, University of Louisville School of Dentistry, Louisville, Kentucky

Received 24 October 2007/ Returned for modification 29 November 2007/ Accepted 26 February 2008

Periodontitis is a chronic human inflammatory disease initiated and sustained by dental plaque microorganisms. A major contributing pathogen is Porphyromonas gingivalis, a gram-negative bacterium recognized by Toll-like receptor 2 (TLR2) and TLR4, which are expressed by human gingival epithelial cells (HGECs). However, it is still unclear how these cells respond to P. gingivalis and initiate inflammatory and immune responses. We have reported previously that HGECs produce a wide range of proinflammatory cytokines, including interleukin-6 (IL-6), IL-8, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor alpha (TNF-{alpha}), and IL-1β. In this study, we show that IL-1β has a special role in the modulation of other inflammatory cytokines in HGECs challenged with P. gingivalis. Our results show that the increased production of IL-1β correlates with the cell surface expression of TLR4, and more specifically, TLR4-normal HGECs produce fourfold more IL-1β than do TLR4-deficient HGECs after challenge. Moreover, blocking the IL-1β receptor greatly reduces the production of "secondary" proinflammatory cytokines such as IL-8 or IL-6. Our data indicate that the induction of IL-1β plays an important role in mediating the release of other proinflammatory cytokines from primary human epithelial cells following challenge with P. gingivalis, and this process may be an inflammatory enhancement mechanism adopted by epithelial cells.

* Corresponding author. Mailing address: University of Louisville School of Dentistry, 501 South Preston Street, Room 204, Louisville, KY 40292. Phone: (502) 852-3175. Fax: (502) 852-5572. E-mail: dfkina01{at}gwise.louisville.edu

{triangledown} Published ahead of print on 10 March 2008.

Editor: B. A. McCormick

Infection and Immunity, May 2008, p. 2080-2089, Vol. 76, No. 5
0019-9567/08/$08.00+0     doi:10.1128/IAI.01428-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Benakanakere, M. R., Li, Q., Eskan, M. A., Singh, A. V., Zhao, J., Galicia, J. C., Stathopoulou, P., Knudsen, T. B., Kinane, D. F. (2009). Modulation of TLR2 Protein Expression by miR-105 in Human Oral Keratinocytes. J. Biol. Chem. 284: 23107-23115 [Abstract] [Full Text]  


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