Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
Department of Biomedical Sciences, University of Padua, Padua, Italy.
Sci Rep. 2017 Jan 11;7:40515. doi: 10.1038/srep40515.
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.
最近的研究表明，某些特定的微生物感染通过诱导炎症和免疫反应参与动脉粥样硬化，但涉及这种病理学的病原体如何引发宿主反应尚不清楚。在这项研究中，我们表明，弯曲杆菌（Hc）是一种与动脉粥样硬化发展相关的人类病原体，因为至少 27%的动脉粥样硬化患者的血清特异性识别 Hc 蛋白质组中的一种蛋白，我们将其命名为弯曲杆菌动脉粥样硬化炎症蛋白（CAIP）（n=71）。CAIP 似乎与这种病理学有关，因为从动脉粥样硬化患者中分离出的动脉粥样硬化斑块富含 CAIP 特异性 T 细胞（10%），我们进一步表明这些 T 细胞驱动 Th1 炎症，这是一种通常与动脉粥样硬化相关的免疫病理反应。重组 CAIP 促进了人巨噬细胞的促炎表型的分化和维持，并触发了泡沫细胞的形成，这是动脉粥样硬化的一个标志。这项研究确定 CAIP 是与 Hc 感染相关的动脉粥样硬化炎症的一个相关因素，并表明预防和根除 Hc 感染可以降低动脉粥样硬化的发生率。
