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Salmonella-Infected Aortic Aneurysm: Investigating Pathogenesis Using Salmonella Serotypes

机译:沙门氏菌感染的主动脉瘤:使用沙门氏菌血清型调查发病机理。

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摘要

infection is most common in patients with infected aortic aneurysm, especially in Asia. When the aortic wall is heavily atherosclerotic, the intima is vulnerable to invasion by , leading to the development of infected aortic aneurysm. By using THP-1 macrophage-derived foam cells to mimic atherosclerosis, we investigated the role of three serotypes – Typhimurium, Enteritidis, and Choleraesuis – in foam cell autophagy and inflammasome formation. Herein, we provide possible pathogenesis of -associated infected aortic aneurysms. Three serotypes with or without virulence plasmid were studied. Through Western blotting, we investigated cell autophagy induction and inflammasome formation in -infected THP-1 macrophage-derived foam cells, detected CD36 expression after infection through flow cytometry, and measured interleukin (IL)-1β, IL-12, and interferon (IFN)-α levels through enzyme-linked immunosorbent assay. At 0.5 h after infection, plasmid-bearing . Enteritidis OU7130 induced the highest foam cell autophagy – significantly higher than that induced by plasmid-less OU7067. However, plasmid-bearing Choleraesuis induced less foam cell autophagy than did its plasmid-less strain. In foam cells, plasmid-less infection (particularly . Choleraesuis OU7266 infection) led to higher CD36 expression than did plasmid-bearing strains infection. OU7130 and OU7266 infection induced the highest IL-1β secretion. OU7067-infected foam cells secreted the highest IL-12p35 level. Plasmid-bearing Typhimurium OU5045 induced a higher IFN-α level than did other serotypes. serotypes are correlated with foam cell autophagy and IL-1β secretion. may affect the course of foam cells formation, or even aortic aneurysm, through autophagy.
机译:感染在主动脉瘤感染患者中最为常见,尤其是在亚洲。当主动脉壁严重动脉粥样硬化时,内膜容易受到侵袭,导致受感染的主动脉瘤的发展。通过使用THP-1巨噬细胞衍生的泡沫细胞模拟动脉粥样硬化,我们研究了三种血清型(鼠伤寒,肠炎和霍乱)在泡沫细胞自噬和炎症小体形成中的作用。在此,我们提供了相关的感染性主动脉瘤的可能发病机制。研究了三种带有或不带有毒力质粒的血清型。通过蛋白质印迹,我们调查了感染的THP-1巨噬细胞衍生的泡沫细胞中的细胞自噬诱导和炎性体形成,通过流式细胞仪检测感染后CD36的表达,并测量白介素(IL)-1β,IL-12和干扰素(IFN)酶联免疫吸附法测定)-α水平。感染后0.5小时,携带质粒。肠炎沙门氏菌OU7130诱导了最高的泡沫细胞自噬,明显高于无质粒的OU7067诱导的自噬。然而,与无质粒菌株相比,带有质粒的霍乱弧菌诱导的泡沫细胞自噬更少。在泡沫细胞中,与无质粒感染相比,无质粒感染(特别是霍乱OU7266感染)导致更高的CD36表达。 OU7130和OU7266感染诱导了最高的IL-1β分泌。 OU7067感染的泡沫细胞分泌最高的IL-12p35水平。携带质粒的鼠伤寒OU5045诱导的IFN-α水平高于其他血清型。血清型与泡沫细胞自噬和IL-1β分泌相关。通过自噬可能会影响泡沫细胞形成的过程,甚至影响主动脉瘤。

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