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Infection and Immunity, September 1998, p. 4056-4060, Vol. 66, No. 9
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Porphyromonas gingivalis Fimbriae Use beta 2 Integrin (CD11/CD18) on Mouse Peritoneal Macrophages as a Cellular Receptor, and the CD18 beta  Chain Plays a Functional Role in Fimbrial Signaling

Akira Takeshita,1 Yukio Murakami,2 Yoshinori Yamashita,1 Masami Ishida,1 Seiichiro Fujisawa,2 Shigeo Kitano,1 and Shigemasa Hanazawa1,*

Departments of Oral Microbiology1 and Oral Diagnosis,2 Meikai University School of Dentistry, Keyakidai, Sakado City, Saitama 350-0283, Japan

Received 7 November 1997/Returned for modification 8 January 1998/Accepted 1 June 1998

In this study, we demonstrate that Porphyromonas gingivalis fimbriae use molecules of beta 2 integrin (CD11/CD18) on mouse peritoneal macrophages as cellular receptors and also show that the beta  chain (CD18) may play a functional role in signalling for the fimbria-induced expression of interleukin-1beta (IL-1beta ) and tumor necrosis factor alpha (TNF-alpha ) genes in the cells. Using a binding assay with 125I-labeled fimbriae, we observed that fimbrial binding to the macrophages was inhibited by treatment with CD11a, CD11b, CD11c, or CD18 antibody but not by that with CD29 antibody. Western blot assays showed that the fimbriae bound to molecules of beta 2 integrin (CD11/CD18) on the macrophages. Furthermore, Northern blot analyses showed that the fimbria-induced expression of IL-1beta and TNF-alpha genes in the cells was inhibited strongly by CD18 antibody treatment and slightly by CD11a, CD11b, or CD11c antibody treatment. Interestingly, intracellular adhesion molecule 1 (ICAM-1), a ligand of CD11/CD18, inhibited fimbrial binding to the cells in a dose-dependent manner. In addition, ICAM-1 clearly inhibited the fimbria-induced expression of IL-1beta and TNF-alpha genes in the cells. However, such inhibitory action was not observed with laminin treatment. These results suggest the importance of beta 2 integrin (CD11/CD18) as a cellular receptor of P. gingivalis fimbriae in the initiation stage of the pathogenic mechanism of the organism in periodontal disease.

* Corresponding author. Mailing address: Department of Oral Microbiology, Meikai University School of Dentistry, Keyakidai, Sakado City, Saitama 350-0283, Japan. Phone: 492-85-5511. Fax: 492-87-6657. E-mail: hanazawa{at}dent.meikai.ac.jp.

Infection and Immunity, September 1998, p. 4056-4060, Vol. 66, No. 9
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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