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Infection and Immunity, February 1999, p. 928-935, Vol. 67, No. 2
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Fas-FasL Interaction Involved in Pathogenesis of Ocular Toxoplasmosis in Mice

Mark S. Hu,1,* Joseph D. Schwartzman,2 Grant R. Yeaman,3 Jane Collins,3 Rosanne Seguin,1 Imtiaz A. Khan,1 and Lloyd H. Kasper1,3

Departments of Medicine,1 Pathology,2 and Microbiology,3 Dartmouth Medical School, Lebanon, New Hampshire 03756

Received 13 July 1998/Returned for modification 28 August 1998/Accepted 5 November 1998

Ocular toxoplasmosis is a potentially blinding intraocular inflammation. The intent of this study was to investigate the role of Fas-FasL interaction in a murine model of acquired ocular toxoplasmosis induced by intracameral inoculation of Toxoplasma gondii. Intraocular inflammation, Fas and FasL expression on lymphocytes and on ocular tissues, the occurrence of apoptosis, and the frequency of CD8+ and CD4+ T cells in the infected eyes were analyzed in C57BL/6 (B6) mice. Susceptibility to parasite-induced intraocular inflammation was observed in Fas-deficient (B6-lpr) and FasL-deficient (B6-gld) mice. Inoculation of 5,000 T. gondii tachyzoites induced significant intraocular inflammation associated with increase of Fas and FasL expression in the inoculated eyes of wild-type B6 mice. Flow cytometry demonstrated a significant increase of Fas and FasL expression on the splenocytes from naive mice incubated in vitro with the parasite and on the splenocytes harvested from the infected mice at day 8 after parasite inoculation. Apoptosis of inflammatory cells and cells in ocular tissues was seen, and a greater frequency of CD8+ than CD4+ T cells was observed in the infected eyes. The intensity of intraocular inflammation was greater in B6-lpr and B6-gld mice than in wild-type B6 mice (P < 0.05). The results suggest that Fas-FasL interaction associated with apoptosis is involved in the pathogenesis of acquired ocular toxoplasmosis in mice.

* Corresponding author. Mailing address: 644E Borwell Research Building, Department of Medicine, Dartmouth Medical School, One Medical Center Dr., Lebanon, NH 03756. Phone: (603) 650-8384. Fax: (603) 650-6841. E-mail: Mark.S.Hu{at}Dartmouth.EDU.

Infection and Immunity, February 1999, p. 928-935, Vol. 67, No. 2
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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