Helicobacter cinaedi infection promotes atherosclerosis

Atherosclerosis is a chronic inflammatory disease, mainly driven by both innate and adaptive immune responses. However, the initiating factor in this chronic inflammation in atherosclerotic tissues remains poorly characterized.

A recent article published in Nature reported that Helicobacter cinaedi infection significantly enhanced atherosclerosis in hyperlipidaemic mice, with macrophage-driven proinflammatory responses involved. (2014 Sci Rep. 4, 4680). 

The abstract reads:

“Helicobacter cinaedi is the most common enterohepatic Helicobacter species that causes bacteremia in humans, but its pathogenicity is unclear. Here, we investigated the possible association of H. cinaedi with atherosclerosis in vivo and in vitro. We found that H. cinaedi infection significantly enhanced atherosclerosis in hyperlipidaemic mice. Aortic root lesions in infected mice showed increased accumulation of neutrophils and F4/80(+) foam cells, which was due, at least partly, to bacteria-mediated increased expression of proinflammatory genes. Although infection was asymptomatic, detection of cytolethal distending toxin RNA of H. cinaedi indicated aorta infection. H. cinaedi infection altered expression of cholesterol receptors and transporters in cultured macrophages and caused foam cell formation. Also, infection induced differentiation of THP-1 monocytes. These data provide the first evidence of a pathogenic role of H. cinaedi in atherosclerosis in experimental models, thereby justifying additional investigations of the possible role of enterohepatic Helicobacter spp. in atherosclerosis and cardiovascular disease. ”

Posted by Tim Sandle