Promotion of atherosclerosis by Helicobacter cinaedi infection that involves macrophage-driven proinflammatory responses

Shahzada Khan, H. N.Ashiqur Rahman, Tatsuya Okamoto, Tetsuro Matsunaga, Yukio Fujiwara, Tomohiro Sawa, Jun Yoshitake, Katsuhiko Ono, Khandaker Ahtesham Ahmed, Md Mizanur Rahaman, Kohta Oyama, Motohiro Takeya, Tomoaki Ida, Yoshiaki Kawamura, Shigemoto Fujii, Takaaki Akaike

Research output: Contribution to journalArticlepeer-review

29 Citations (Scopus)

Abstract

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.

Original languageEnglish
Article number4680
JournalScientific reports
Volume4
DOIs
Publication statusPublished - 2014

ASJC Scopus subject areas

  • General

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