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
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