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Infection and Immunity, May 2002, p. 2559-2565, Vol. 70, No. 5
0019-9567/02/$04.00+0 DOI: 10.1128/IAI.70.5.2559-2565.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Unité de Biologie Moléculaire du Gène, INSERM U277, Université Paris 7,1 Unité de Biologie des Interactions Cellulaires, URA CNRS 1960, Institut Pasteur, 75724 Paris Cedex 15, France,3 Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 722052
Received 16 July 2001/ Returned for modification 31 August 2001/ Accepted 25 January 2002
The effect of gamma interferon (IFN-
) on apoptosis due to infection by Chlamydia muridarum (the mouse pneumonitis strain of Chlamydia trachomatis) was studied in epithelial cells in culture and in the genital tracts of mice. IFN-
concentrations that induce the formation of aberrant, persistent chlamydiae inhibit apoptosis due to C. muridarum infection. In cells treated with an IFN-
concentration that leads to the development of a heterogenous population of normal and aberrant Chlamydia vacuoles, apoptosis was inhibited preferentially in cells that contained the aberrant vacuoles. The inhibitory effect of IFN-
appears to be due in part to expression of host cell indoleamine 2,3-dioxygenase activity, since inhibition of apoptosis could be partially reversed through coincubation with exogenous tryptophan. Apoptotic cells were observed in the genital tracts of wild-type mice infected with C. muridarum, and a significantly larger number of apoptotic cells was detected in infected IFN-
-deficient mice. These results suggest that IFN-
may contribute to pathogenesis of persistent Chlamydia infections in vivo by preventing apoptosis of infected cells.
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