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J. Med. Microbiol. -- Vol. 51 (2002), 27-33
© 2002 Society for General Microbiology
ISSN 0022-2615


BACTERIAL PATHOGENICITY

Activation of human gingival epithelial cells by cell-surface components of black-pigmented bacteria: augmentation of production of interleukin-8, granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor and expression of intercellular adhesion molecule 1

A. SUGIYAMA, A. UEHARA, K. IKI{dagger}, K. MATSUSHITA{dagger}, R. NAKAMURA*, T. OGAWA{ddagger}, S. SUGAWARA and H. TAKADA

Department of Microbiology and Immunology, Tohoku University School of Dentistry, Sendai 980-8575, *Department of Preventive Dentistry, University of Tokushima School of Dentistry, Tokushima 770-8504, {dagger}Departments of Biochemistry, Periodontology and Operative Dentistry and Endodontology, Kagoshima University Dental School, Kagoshima 890-8544 and {ddagger}Department of Oral Microbiology, Asahi University School of Dentistry, Gifu 501-0296, Japan

Corresponding author: Professor H. Takada (e-mail: dent-ht{at}mail.cc.thoku.ac.jp).

Received 9 Jan. 2001; revised version received 30 May 2001; accepted 20 June 2001.

Abstract

Black-pigmented anaerobic bacteria, such as Porphyromonas gingivalis and Prevotella intermedia, are amongst the predominant bacteria in periodontal pockets and have been implicated in periodontal diseases. To elucidate the roles of gingival keratinocytes, which are the first cells encountered by oral bacteria in periodontal diseases, human gingival keratinocytes in primary culture were stimulated with cell-surface components of P. gingivalis and Pr. intermedia. A glycoprotein fraction from Pr. intermedia (PGP) clearly augmented the release of interleukin-8, granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor, as determined by enzyme-linked immunosorbent assay. This PGP also induced expression of intercellular adhesion molecule-1 (ICAM-1), as determined by flow cytometry. The augmentation of mRNA expression for these molecules was also confirmed by reverse transcription PCR. In contrast, lipopolysaccharide (LPS) from Pr. intermedia and Escherichia coli was completely inactive in these assays. LPS fraction and purified fimbriae from P. gingivalis exhibited weak activities. Cytokine production and ICAM-1 expression by gingival keratinocytes might cause accumulation and activation of neutrophils in the epithelium and, therefore, may be involved in the initiation and development of inflammation in periodontal tissues.




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