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Infection and Immunity, October 2004, p. 5947-5954, Vol. 72, No. 10
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.10.5947-5954.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Role of Cell-Cell Communication in Inhibiting Butyric Acid-Induced T-Cell Apoptosis

Tomoko Kurita-Ochiai,1* Shintaro Seto,2 and Kuniyasu Ochiai2

Department of Microbiology, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba,1 Department of Oral Microbiology, Meikai University School of Dentistry, Sakado, Saitama, Japan2

Received 1 March 2004/ Returned for modification 15 April 2004/ Accepted 5 July 2004

We have previously demonstrated that human gingival fibroblasts rescue butyric acid-induced T-cell apoptosis via proinflammatory cytokines such as interleukin 6 (IL-6) and IL-11, which are produced by fibroblasts stimulated with butyric acid. In this study, we determined if T-cell adhesion to human gingival fibroblasts influenced the susceptibility of T cells to butyric acid-induced apoptosis. We have shown that the number of Jurkat T cells adherent to gingival fibroblasts (Gin-1 cells) was significantly increased by the addition of butyric acid. All Jurkat cells that adhered to Gin-1 cells remained viable, while the nonadherent Jurkat cells dropped into apoptosis. The increase in T-cell adhesion to fibroblasts was also observed when Jurkat cells, but not Gin-1 cells, were pretreated with butyric acid. The expression levels of CD44, very late antigen 2 (VLA-2) and VLA-5 but not of leukocyte function-associated antigen 1 (LFA-1) and VLA-4 on Jurkat cells were increased following treatment with butyric acid. Furthermore, pretreatment of butyric acid-sensitized Jurkat cells with monoclonal antibodies against CD44, VLA-2, and VLA-5, but not LFA-1 and VLA-4, followed by coculture with Gin-1 cells inhibited T-cell adhesion to fibroblasts and increased apoptosis of nonadherent T cells after coculture of gingival fibroblasts and Jurkat cells. These results indicate that T-cell adherence to fibroblasts is enhanced by butyric acid and that butyric acid-induced T-cell apoptosis is down-regulated by T-cell adhesion to gingival fibroblasts through an interaction with the adhesion molecules CD44, VLA-2, and VLA-5 expressed on T cells stimulated with butyric acid.

* Corresponding author. Mailing address: Department of Microbiology, Nihon University School of Dentistry at Matsudo, Matsudo-shi, Chiba 271–8587, Japan. Phone: 47 360 9342. Fax: 47 360 9343. E-mail: tkurita{at}mascat.nihon-u.ac.jp.

Editor: J. D. Clements

Infection and Immunity, October 2004, p. 5947-5954, Vol. 72, No. 10
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.10.5947-5954.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.





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