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Caspase-1 Activation Is Related With HIV-Associated Atherosclerosis in an HIV Transgenic Mouse Model and HIV Patient Cohort.

著者 Kearns AC , Liu F , Dai S , Robinson JA , Kiernan E , Tesfaye Cheru L , Peng X , Gordon J , Morgello S , Abuova A , Lo J , Zanni MV , Grinspoon S , Burdo TH , Qin X
Arterioscler Thromb Vasc Biol.2019 Jul 18 ; ():ATVBAHA119312603.
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Atherosclerotic cardiovascular disease (ASCVD) is an increasing cause of morbidity and mortality in patients with HIV since the introduction of combination antiretroviral therapy. Despite recent advances in our understanding of HIV ASCVD, controversy still exists on whether this increased risk of ASCVD is due to chronic HIV infection or other risk factors. Mounting biomarker studies indicate a role of monocyte/macrophage activation in HIV ASCVD; however, little is known about the mechanisms through which HIV infection mediates monocyte/macrophage activation in such a way as to engender accelerated atherogenesis. Here, we experimentally investigated whether HIV expression is sufficient to accelerate atherosclerosis and evaluated the role of caspase-1 activation in monocytes/macrophages in HIV ASCVD. Approach and Results: We crossed a well-characterized HIV mouse model, Tg26 mice, which transgenically expresses HIV-1, with ApoE mice to promote atherogenic conditions (Tg26/ApoE). Tg26/ApoE have accelerated atherosclerosis with increased caspase-1 pathway activation in inflammatory monocytes and atherosclerotic vasculature compared with ApoE. Using a well-characterized cohort of patients with HIV and tissue-banked aortic plaques, we documented that serum IL (interleukin)-18 was higher in patients with HIV compared with non-HIV-infected controls, and in patients with plaques, IL-18 levels correlated with monocyte/macrophage activation markers and noncalcified inflammatory plaques. In autopsy-derived aortic plaques, caspase-1+ cells and CD163+ macrophages correlated.
PMID: 31315440 [PubMed - as supplied by publisher]
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