ArticleScientific reports2017
The Helicobacter cinaedi antigen CAIP participates in atherosclerotic inflammation by promoting the differentiation of macrophages in foam cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- CD300e modulates metabolic programs in adipose tissue macrophages during obesity.Cell death & disease · 2026Article
- Changes in potential pathogenicity-associated proteins ofFrontiers in microbiology · 2025Article
- CAIP-Induced ROS Production Contributes to Sustaining Atherosclerotic Process Associated withInternational journal of molecular sciences · 2024Article
- Review
- Article
- HP-NAP ofFrontiers in immunology · 2022Review
- Acquired Hemophilia A Presenting with Infectious Aortic Aneurysms Due to an Underlying Helicobacter cinaedi Infection.Internal medicine (Tokyo, Japan) · 2021Article
- Tumor Cells and the Extracellular Matrix Dictate the Pro-Tumoral Profile of Macrophages in CRC.Cancers · 2021Article
- Phagocytosis of polymeric nanoparticles aided activation of macrophages to increase atherosclerotic plaques in ApoEJournal of nanobiotechnology · 2021Article
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have shown that certain specific microbial infections participate in atherosclerosis by inducing inflammation and immune reactions, but how the pathogens implicated in this pathology trigger the host responses remains unknown. In this study we show that Helicobacter cinaedi (Hc) is a human pathogen linked to atherosclerosis development since at least 27% of sera from atherosclerotic patients specifically recognize a protein of the Hc proteome, that we named Cinaedi Atherosclerosis Inflammatory Protein (CAIP) (n = 71). CAIP appears to be implicated in this pathology because atheromatous plaques isolated from atherosclerotic patients are enriched in CAIP-specific T cells (10%) which, in turn, we show to drive a Th1 inflammation, an immunopathological response typically associated to atherosclerosis. Recombinant CAIP promotes the differentiation and maintenance of the pro-inflammatory profile of human macrophages and triggers the formation of foam cells, which are a hallmark of atherosclerosis. This study identifies CAIP as a relevant factor in atherosclerosis inflammation linked to Hc infection and suggests that preventing and eradicating Hc infection could reduce the incidence of atherosclerosis.
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