Chlamydia trachomatis(Mouse Pneumonitis Strain) Induces Cardiovascular Pathology following Respiratory Tract Infection

Abstract

Chlamydia, especially Chlamydia pneumoniae, infection is closely associated with human cardiovascular diseases. Thus far, however, few experimental studies have been carried out to investigate whether natural C. trachomatis infection can induce cardiovascular pathological changes. In this article, we report that pulmonary infection with C. trachomatis mouse pneumonitis strain (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 multiple organs including the cardiovascular tissues. In addition, gamma interferon 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 respiratory tract infection may be a useful experimental model for investigating cardiovascular diseases caused by chlamydial infection.

Myocardial Inflammation in Autoimmune Diseases: Investigation by Cardiovascular Magnetic Resonance and Endomyocardial Biopsy

“…Myocarditis occurs when the host fails to control the infection. Under these circumstances, the real prevalence of Chlamydia-induced myocarditis may be higher than previously documented [33]. Infection with Chlamydia trachomatis leads to production of autoantibodies to heart muscle-specific epitopes and Chlamydia-mediated heart disease is induced [34].…”

Myocarditis as a precipitating factor for heart failure: evaluation and 1‐year follow‐up using cardiovascular magnetic resonance and endomyocardial biopsy

“…Myocarditis occurs when the host fails to control the infection. Under these circumstances, the real prevalence of Chlamydia‐induced myocarditis may be higher than previously documented 37. It leads to the production of heart muscle‐specific epitopes autoantibodies and Chlamydia‐mediated heart disease 38…”

CFTR is required for cellular entry and internalization of Chlamydia trachomatis

“…C. trachomatis, as well as infections in both male and female reproductive tracts, are the most common sexually transmitted disease. C. trachomatis infections have also been implicated in the aetiology of heart diseases (Fan et al, 1999), as well as cofactor for many microbes including viruses such as HIV (Peters et al, 1995), HPV (human papilloma virus) (Smith et al, 2002) and most recently, the lethal SARS (severe acute respiratory syndrome) virus (Hong et al, 2003).…”