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BACTERIAL PATHOGENICITY |
Department of Conservative Dentistry, Tokushima University School of Dentistry, Tokushima 770-8504 and *Department of Restorative Dentistry and Endodontology, Osaka University Graduate School of Dentistry, Osaka 565-0871, Japan
Corresponding author: Dr H. Nakae (e-mail: nakae{at}dent.dent.tokushima-u.ac.jp).
Received 27 March 2002; accepted 1 June 2002.
During the acute inflammatory response in periodontitis, gingival epithelial cells are considered to play important roles in the recruitment of inflammatory cells to the site of infection through the secretion of chemokines. However, little is known about the expression of molecules that are involved in the interaction between the epithelium and neutrophils following bacterial attachment. Earlier work reported that periodontopathogenic Eikenella corrodens strain 1073 up-regulated the expression and secretion of chemokines such as interleukin-8 (IL-8) from KB cells (a human oral epithelial cell line derived from a human oral epidermoid carcinoma). To elucidate the mechanism of the transmigration of neutrophils through the epithelium, the present study investigated the expression of adhesion molecules on KB cells in response to E. corrodens attachment. Adhesion molecule gene expression was assessed by RT-PCR and adhesion proteins expressed on KB cell surfaces were determined by cell-based ELISA and FACS. In RT-PCR, ICAM-1 mRNA levels were significantly increased within 1 h in response to exposure to E. corrodens and continued to increase over the 12-h period of study. In ELISA, increased surface ICAM-1 expression was paralleled by increased ICAM-1 mRNA levels. Furthermore, the increases in ICAM-1 expression on epithelial cells infected with E. corrodens were observed to be due to the N-acetyl-D-galactosamine (GalNAc) specific bacterial lectin-like substance of E. corrodens (EcLS), which was one of the adhesins of E. corrodens. This is the first study to report that a bacterial lectin-like substance increased the expression of ICAM-1 on gingival epithelial cells.
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