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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-gamma) 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-gamma treatment. IDO-mediated increase in tryptophan catabolism resulted in a dose-dependent marked inhibition of C. pneumoniae replication.

infection and immunity

Inhibition of <i>Chlamydia pneumoniae</i> Replication in Human Aortic Smooth Muscle Cells by Gamma Interferon-Induced Indoleamine 2,3-Dioxygenase Activity

Inhibition of Chlamydia pneumoniae Replication in Human Aortic Smooth Muscle Cells by Gamma Interferon-Induced Indoleamine 2,3-Dioxygenase Activity