The Helicobacter cinaedi antigen CAIP participates in atherosclerotic inflammation by promoting the differentiation of macrophages in foam cells

Recent studies have shown that certain speci c microbial infections participate in atherosclerosis by inducing in ammation 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 speci cally recognize a protein of the Hc proteome, that we named Cinaedi Atherosclerosis In ammatory Protein (CAIP) (n = 71). CAIP appears to be implicated in this pathology because atheromatous plaques isolated from atherosclerotic patients are enriched in CAIP-speci c T cells (10%) which, in turn, we show to drive a Th1 in ammation, an immunopathological response typically associated to atherosclerosis. Recombinant CAIP promotes the di erentiation and maintenance of the pro-in ammatory pro le of human macrophages and triggers the formation of foam cells, which are a hallmark of atherosclerosis. This study identi es CAIP as a relevant factor in atherosclerosis in ammation linked to Hc infection and suggests that preventing and eradicating Hc infection could reduce the incidence of atherosclerosis.