Inhibition of Chlamydia pneumoniae replication in human aortic smooth muscle cells by gamma interferon-induced indoleamine 2, 3-dioxygenase activity.
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.
Pantoja
L G
LG
Division of Infectious Diseases, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky 40292, USA.
Miller
R D
RD
Ramirez
J A
JA
Molestina
R E
RE
Summersgill
J T
JT
D001011:Aorta / Q000382:microbiology*; D001161:Arteriosclerosis / Q000209:etiology; D002478:Cells, Cultured; D016993:Chlamydophila pneumoniae / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase; D007371:Interferon-gamma / Q000494:pharmacology*; D009131:Muscle, Smooth, Vascular / Q000382:microbiology*; D014366:Tryptophan Oxygenase / Q000502:physiology*
D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase; D007371:Interferon-gamma; D014366:Tryptophan Oxygenase