Chlamydia, especially Chlamydia pneumoniae, infection is closely associated
with human cardiovascular diseases. Thus far, however, few experimental st
udies have been carried out to investigate whether natural C. trachomatis i
nfection can induce cardiovascular pathological changes. In this article, w
e report that pulmonary infection with C. trachomatis mouse pneumonitis str
ain (MoPn) can induce myocardial and perivascular inflammation and fibrosis
in C57BL/6 mice. The pulmonary MoPn infection appeared to be disseminated
systemically, because chlamydial antigens were readily detectable in multip
le organs including the cardiovascular tissues. In addition, gamma interfer
on gene knockout mice with a C57BL/6 genetic background showed significant
endocarditis and pancarditis characterized by vegetation in aortic valves,
interstitial and pericardial inflammatory cellular infiltration, and growth
of the organisms in the heart following respiratory tract MoPn infection.
The results indicate that C. trachomatis can induce cardiovascular diseases
following respiratory tract infection and suggest that murine MoPn respira
tory tract infection may be a useful experimental model for investigating c
ardiovascular diseases caused by chlamydial infection.