MedWire News: Co-infection with Chlamydia pneumoniae and human cytomegalovirus (HCMV) stimulates greater expression of inflammatory factors in aortic smooth muscle cells than either infection alone, show study findings.
Dirk Prochnau (Friedrich Schiller University, Jena, Germany) and colleagues believe that their findings indicate a "novel molecular link between infection and vascular disease development."
Bacterial and viral infections such as C. pneumoniae and HCMV have previously been linked to atherosclerosis. Research suggests that C. pneumoniae "may contribute to native atherosclerosis by inducing chronic inflammation during persistence in atherosclerotic plaques," whereas HCMV has been largely associated with accelerated graft atherosclerosis.
Prochnau and team assessed whether co-infection with both these pathogens may have a supra-additive effect on risk for atherosclerosis.
As reported in the Canadian Journal of Infectious Diseases and Medical Microbiology, they evaluated levels of the inflammatory factors interleukin (IL)-6, IL-8, basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF)-AA, and regulated on activation normal T-cell expressed and secreted (RANTES) in co-infected aortic smooth muscle cells. Cells infected with C. pneumoniae and HCMV alone were also tested for comparison purposes.
Infection with each pathogen alone stimulated IL-6, IL-8, RANTES, and bFGF expression in a dose- and time-dependent manner, although only infection with HCMV stimulated PDGF-AA expression.
Aortic cells that were co-infected with both pathogens had significantly higher expression levels of the inflammatory factors tested.
More specifically, expression of IL-6 was increased by 30% in co-infected compared with in C. pneumoniae or HCMV infected cells at 48 hours of infection. Similarly, IL-8 expression was increased by 137% at 24 hours and bFGF expression by 209% at 48 hours after co-infection compared with after single-pathogen infection.
However, no additional expression of RANTES or PDGF-AA was observed after co- as opposed to single-infection.
"Our findings support the hypothesis that the cumulative burden of pathogens such as C. pneumoniae and HCMV may contribute to the growth and destabilization of atherosclerotic plaques, and provide a possible molecular link between infection and vascular disease development," conclude Prochnau and co-authors.
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