Plasma Inflammatory Biomarkers Associated with Advanced Liver Fibrosis in HIV-HCV-Coinfected Individuals.

Plasma Inflammatory Biomarkers Associated with Advanced Liver Fibrosis in HIV-HCV-Coinfected Individuals.
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DOI:
10.3390/ijerph17249474
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发表时间:
2020-12-17
影响因子:
--
通讯作者:
He N
He N
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Chen X;Liu X;Duan S;Tang R;Zhou S;Ye R;Yang Y;Wang J;Yao S;He N

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背景资料:HIV和HCV合并感染可加速肝纤维化,其中微生物易位和全身炎症可能起重要作用。目的:本研究的目的是提供一个广泛的资料,血浆微生物易位和炎症生物标志物与晚期肝纤维化之间的艾滋病毒和丙型肝炎病毒合并感染的患者。研究方法:这项横断面研究从中国西南部云南省的一个农村地区招募了343名接受联合抗逆转录病毒治疗(cART)的HIV-HCV合并感染患者。测定血浆sCD 14和27种细胞因子和趋化因子的浓度,并与晚期或轻度肝纤维化水平进行比较。结果:343例HIV-HCV合并感染患者中,188例(54.8%)有重度或晚期肝纤维化(FIB-4 > 3.25)。晚期肝纤维化患者(FIB-4 > 3.25 vs. FIB-4 ≤ 3.25)的白细胞介素(IL)-1β、IL-6、IL-7、IL-9、IL-12、IL-15、IL-17、粒细胞巨噬细胞集落刺激因子(GM-CSF)、干扰素-γ(IFN-γ)、肿瘤坏死因子(TNF-α)、IL-4、IL-10、IL-13、成纤维细胞生长因子2(碱性FGF)和单核细胞趋化蛋白-1(MCP-1)。多变量逻辑回归模型显示,晚期肝纤维化与IL-1β、IL-6、IL-7、IL-12、IL-17、GM-CSF、IFN-γ、IL-4、IL-10、MCP-1、Eotaxin和FGF-碱性的血浆水平升高相关,FGF-碱性继续与晚期肝纤维化正相关且显著相关,经Bonferroni校正后进行多重比较(校正后比值比(aOR)= 1.92; 95%CI:1.32-2.81; p = 0.001)。血浆sCD 14也与晚期肝纤维化显著相关(aOR = 1.13; 95%CI:1.01-1.30; p = 0.049)。结论:HIV-HCV合并感染的患者生活在晚期肝纤维化的高患病率中,其与升高的血浆炎症和微生物易位生物标志物的混合物共存。FGF-basic和sCD 14与肝纤维化的显著相关性可能揭示HCV-HIV合并感染肝纤维化的致病机制和潜在的临床干预靶点。
Background: HIV and HCV coinfection leads to accelerated liver fibrosis, in which microbial translocation and systemic inflammation might play important roles. Objective: This study aimed to provide an extensive profile of the plasma microbial translocation and inflammation biomarkers associated with advanced liver fibrosis among HIV–HCV-coinfected patients. Methods: This cross-sectional study recruited 343 HIV–HCV-coinfected patients on combination antiretroviral therapy (cART) from a rural prefecture of Yunnan province in Southwest China. The plasma concentrations of sCD14 and 27 cytokines and chemokines were assayed and compared against advanced or mild levels of liver fibrosis. Results: Of the 343 HIV–HCV-coinfected patients, 188 (54.8%) had severe or advanced liver fibrosis (FIB-4 > 3.25). The patients with advanced liver fibrosis (FIB-4 > 3.25 vs. FIB-4 ≤ 3.25) had higher plasma levels of interleukin (IL)-1β, IL-6, IL-7, IL-9, IL-12, IL-15, IL-17, granulocyte macrophage colony stimulating factor (GM-CSF), Interferon-γ (IFN-γ), tumor necrosis factor (TNF-α), IL-4, IL-10, IL-13, fibroblast growth factor 2 (FGF-basic), and Monocyte chemoattractant protein-1 (MCP-1). Multivariable logistic regression models showed that advanced liver fibrosis was associated with an increased plasma level of IL-1β, IL-6, IL-7, IL-12, IL-17, GM-CSF, IFN-γ, IL-4, IL-10, MCP-1, Eotaxin, and FGF-basic, with FGF-basic continuing to be positively and significantly associated with advanced liver fibrosis, after Bonferroni correction for multiple comparisons (adjusted odds ratio (aOR) = 1.92; 95%CI: 1.32–2.81; p = 0.001). Plasma sCD14 was also significantly associated with advanced liver fibrosis (aOR = 1.13; 95%CI: 1.01–1.30; p = 0.049). Conclusions: HIV–HCV-coinfected patients are living with a high prevalence of advanced liver fibrosis which coexists with a mixture of elevated plasma inflammation and microbial translocation biomarkers. The significant associations of advanced liver fibrosis with FGF-basic and sCD14 may reveal pathogenic mechanisms and potential clinical intervention targets for liver fibrosis in HCV–HIV coinfection.
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