This Article Full Text (PDF) Other Versions of this Article: IAI.01428-07v1 76/5/2080    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Eskan, M. A Articles by Kinane, D. F Search for Related Content PubMed PubMed Citation Articles by Eskan, M. A Articles by Kinane, D. F

 Previous Article  |  Next Article 

Infect. Immun. doi:10.1128/IAI.01428-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

IL-1 modulates proinflammatory cytokine production in human epithelial cells

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

^* To whom correspondence should be addressed. Email: dfkina01{at}gwise.louisville.edu.

	Abstract

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 (TLR)-2 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 IL-6, IL-8, GM-CSF, TNF- and IL-1. In this study, we show that IL-1 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-1 correlates with the cell surface expression of TLR4 and more specifically TLR4-normal HGECs produce four-fold more IL-1 than TLR4-deficient HGECs following challenge. Moreover, blocking the IL-1 receptor greatly reduces production of ‘secondary' proinflammatory cytokines such as IL-8 or IL-6. Our data indicates that the induction of IL-1 plays an important role in mediating release of other proinflammatory cytokines from primary human epithelial cells following P. gingivalis challenge and this process may be an inflammatory enhancement mechanism adopted by epithelial cells.