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Infection and Immunity, March 1999, p. 1450-1454, Vol. 67, No. 3
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

In Vitro Induction of Activation-Induced Cell Death in Lymphocytes from Chronic Periodontal Lesions by Exogenous Fas Ligand

Takamasa Sawa,dagger Fusanori Nishimura, Hideki Ohyama, Keiso Takahashi, Shogo Takashiba, and Yoji Murayama*

Department of Periodontology and Endodontology, Okayama University Dental School, Okayama, Japan

Received 27 July 1998/Returned for modification 8 September 1998/Accepted 20 November 1998

Periodontitis is a chronic inflammatory disease which gradually destroys the supporting tissues of the teeth, leading to tooth loss in adults. The lesions are characterized by a persistence of inflammatory cells in gingival and periodontal connective tissues. To understand what mechanisms are involved in the establishment of chronic lesions, we hypothesized that infiltrating lymphocytes might be resistant to apoptosis. However, both Bcl-2 and Bcl-xL were weakly detected in lymphocytes from the lesions, compared with those from peripheral blood, suggesting that these cells are susceptible to apoptosis. Nevertheless, very few apoptotic cells were observed in tissue sections from the lesions. Lymphocytes from the lesions expressed mRNA encoding Fas, whereas Fas-ligand mRNA was very weakly expressed in lymphocytes from the lesions and in periodontal tissues. Since the results indicated that lymphocytes in the lesions might be susceptible to Fas-mediated apoptosis but lack the death signal, we next investigated if these lymphocytes actually undergo apoptosis by the addition of anti-Fas antibodies in vitro. Fas-positive lymphocytes from the lesions underwent apoptosis by these antibodies, but Fas-negative lymphocytes and Fas-positive peripheral lymphocytes did not undergo apoptosis by these antibodies. These results indicate that lymphocytes in the lesions are susceptible to activation-induced cell death and are induced to die by apoptosis after the addition of exogenous Fas ligand.

* Corresponding author. Mailing address: Department of Periodontology and Endodontology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700-8525, Japan. Phone: 81-86-235-6675. Fax: 81-86-235-6679. E-mail: murayama{at}dent.okayama-u.ac.jp.

dagger Present address: Department of Periodontology and Endodontology, Tokushima University School of Dentistry, Tokushima 770, Japan.

Infection and Immunity, March 1999, p. 1450-1454, Vol. 67, No. 3
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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