Positive Chlamydia pneumoniae serology is associated with elevated levels of tumor necrosis factor alpha in patients with coronary heart disease

Multiple inflammatory markers in patients with significant coronary artery disease

“…The presence of antibodies to C. pneumoniae was additive to the effect of hypercholesterolemia in the multivariate model, arguing against that the effect should be mainly by promoting a proatherogenic serum lipid profile. It was also additive to neopterin concentrations, indicating that the effect was not solely through macrophage activation as previously suggested [21].…”

Association of Lipopolysaccharide-Binding Protein and Coronary Artery Disease in Men

“…Epidemiologic evidence has suggested a link between microbial infection and atherosclerosis (4 -6). In particular, it is possible that lipopolysaccharide (LPS) from bacteria such as Chlamydia pneumonia (7)(8)(9), Helicobacter pylori (10,11), or Porphyromonas gingivalis (6,12) may be triggering the inflammatory response that leads to atherogenesis. The question that remains is how these microbial pathogens trigger this inflammatory disease.…”

“…Thus it is emerging that LPS from various gram-negative bacteria might lead to the initiation of events that lead to the recruitment of inflammatory cells into atherosclerotic lesions (9,11,18). Many of the steps involved in the interaction of lipopolysaccharides (LPS) with monocytes and endothelial cells have been revealed in the last 2 decades: LPS binds to lipopolysaccharide-binding protein (LBP) (19,20), and LPS/LBP complexes are delivered to CD14 (21) which in turn interacts with TLRs.…”

Divergent modulation of Chlamydia pneumoniae infection cycle in human monocytic and endothelial cells by iron, tryptophan availability and interferon gamma

“…These observations have been traced back to induction of a chronic inflammatory status as a consequence of infection and/or iron overload (Kiechl et al, 2001) with subsequent formation of reactive oxygen species leading to endothelial damage (Griendling and FitzGerald, 2003a). The infection with C. pneumoniae is discussed as a central pathogenic factor of atherosclerosis and as cofactor for the progression of inflammation after the initial damage has been set (Griendling and FitzGerald, 2003b;Schumacher et al, 2002;Videm et al, 2007). This potential causative role of C. pneumoniae and the possible overestimation of chlamydial infection on the other hand is still a matter of controversy (Schumacher et al, 2002;Videm et al, 2007;Leinonen and Saikku, 2002;Ngeh et al, 2002).…”