Description of human AAA by cytokine and immune cell aberrations compared to risk-factor matched controls.
Description of human AAA by cytokine and immune cell aberrations compared to risk-factor matched controls.
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DOI:
10.1016/j.surg.2018.03.002
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发表时间:
2018-08
期刊:
影响因子:
3.8
通讯作者:
Murphy MP
中科院分区:
文献类型:
--
作者:
Wang SK;Green LA;Gutwein AR;Drucker NA;Motaganahalli RL;Gupta AK;Fajardo A;Murphy MP
The pathogenesis driving the formation of abdominal aortic aneurysms (AAA) continues to be poorly understood. Therefore, we systemically define the cytokine and circulating immune cell environment observed in human AAA compared to risk-factor matched (RFM) controls. From 2015 to 2017, 274 patients donated blood to the Indiana University Center for Aortic Disease (IUCAD). Absolute concentrations of circulating cytokines were determined using enzyme-linked immunosorbent assays (ELISA) while expression of circulating immune cell phenotypes were assayed via flow cytometric analysis. Human AAA is characterized by a significant depletion of the antigen-specific, CD4+ Tr1 regulatory lymphocyte which corresponds to an upregulation of the antigen-specific, inflammatory Th17 cell. There were no differences in the incidence of Treg, B10, and myeloid-derived suppressor (MDSC) regulatory cells. Similarly, no disparities were noted in the following inflammatory cytokines: IL-1β, C-reactive protein (CRP), tumor necrosis factor α (TNF-α), interferon γ (IFN-γ), and IL-23. However, significant upregulation of the inflammatory cytokines osteopontin (OPN), IL-6, and IL-17 were noted. Additionally, no changes were observed in the regulatory cytokines IL-2, IL-4, IL-13, TNF-stimulated gene 6 protein (TSG-6), and prostaglandin E2 (PGE2), but we did observe a significant decrease in the essential regulatory cytokine IL-10. In this investigation, we systematically characterize the AAA immune environment and present preliminary evidence that faulty immune regulation may also contribute to aneurysm formation and growth.
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影响因子:
3.7
作者:
Nishihara M;Aoki H;Ohno S;Furusho A;Hirakata S;Nishida N;Ito S;Hayashi M;Imaizumi T;Fukumoto Y
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4.3
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4.4
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通讯作者:
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