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Infection and Immunity, November 2000, p. 6478-6481, Vol. 68, No. 11
Division of Infectious Diseases, Department
of Medicine,1 and Department of
Microbiology and Immunology,2 University of
Louisville School of Medicine, Louisville, Kentucky 40292
Received 20 April 2000/Returned for modification 31 May
2000/Accepted 24 August 2000
Infection with Chlamydia pneumoniae, a human
respiratory pathogen, has been implicated as a potential risk factor in
atherosclerosis, possibly because the pathogen can exist in a
persistent form similar to that described for Chlamydia
trachomatis. The present study investigated whether gamma
interferon (IFN-
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Inhibition of Chlamydia pneumoniae
Replication in Human Aortic Smooth Muscle Cells by Gamma
Interferon-Induced Indoleamine 2,3-Dioxygenase Activity
) can induce indoleamine 2,3-dioxygenase (IDO)
activity in aortic smooth muscle cells, leading to a marked inhibition
of C. pneumoniae growth. Our data indicate a stimulation of
IDO mRNA expression and dose-dependent enzymatic activity following
IFN-
treatment. IDO-mediated increase in tryptophan catabolism
resulted in a dose-dependent marked inhibition of C. pneumoniae replication.
*
Corresponding author. Mailing address: Division of
Infectious Diseases, MDR Building, Room 612, Department of Medicine,
University of Louisville, Louisville, KY 40292. Phone: (502) 852-5132. Fax: (502) 852-1147. E-mail: jtsumm{at}louisville.edu.
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