Institute of Microbiology, Biotechnology and Immunology, Department of Immunology and Infectious Biology, Faculty of Biology and Environmental Protection, University of Lodz, Banacha st 12/16, 90-237 Lodz, Poland.
The Bio-Med-Chem Doctoral School, University of Lodz and Lodz Institutes of the Polish Academy of Sciences, Banacha st 12/16, 90-237 Lodz, Poland.
Int J Mol Sci. 2021 Mar 25;22(7):3394. doi: 10.3390/ijms22073394.
Classic atherosclerosis risk factors do not explain all cases of chronic heart disease. There is significant evidence that gut microbiota may influence the development of atherosclerosis. The widespread prevalence of chronic (, ) infections suggests that can be the source of components that stimulate local and systemic inflammatory responses. Elevated production of reactive oxygen species during infection leads to cholesterol oxidation, which drives atherogenesis. The aim of this study is to explore the link between persistent infection and a high-fat diet in the development of proinflammatory conditions that are potentially proatherogenic. An in vivo model of infected with and exposed to an experimental diet was investigated for the occurrence of a proinflammatory and proatherogenic endothelial environment. Vascular endothelial primary cells exposed to components were tested in vitro for oxidative stress, cell activation and apoptosis. The infiltration of inflammatory cells into the vascular endothelium of animals infected with and exposed to a high-fat diet was observed in conjunction with an increased level of inflammatory markers systemically. The arteries of such animals were the least elastic, suggesting the role of in arterial stiffness. Soluble components induced transformation of macrophages to foam cells in vitro and influenced the endothelial life span, which was correlated with Collagen I upregulation. These preliminary results support the hypothesis that antigens act synergistically with a high-fat diet in the development of proatherogenic conditions.
经典的动脉粥样硬化危险因素并不能解释所有慢性心脏病病例。有大量证据表明，肠道微生物群可能会影响动脉粥样硬化的发展。慢性（，）感染的广泛流行表明，（，）可以成为刺激局部和全身炎症反应的成分的来源。（，）感染期间活性氧的产生增加会导致胆固醇氧化，从而导致动脉粥样硬化形成。本研究旨在探讨持续性（，）感染与高脂肪饮食在发展潜在促动脉粥样硬化的促炎状态中的联系。研究了感染（，）并暴露于实验饮食的体内模型中，以研究发生促炎和促动脉粥样硬化的内皮环境的情况。将血管内皮原代细胞暴露于（，）成分中，在体外测试其氧化应激、细胞激活和细胞凋亡。观察到感染（，）并暴露于高脂肪饮食的动物的血管内皮细胞中有炎症细胞浸润，并伴有全身炎症标志物水平升高。这些动物的动脉弹性最差，表明（，）在动脉僵硬中起作用。可溶性（，）成分在体外诱导巨噬细胞向泡沫细胞转化，并影响内皮细胞寿命，这与 Collagen I 的上调相关。这些初步结果支持这样一种假设，即（，）抗原与高脂肪饮食协同作用，导致促动脉粥样硬化状态的形成。
