S100B and Inflammatory Cytokine Levels in Blood as Potential Markers of Blood-Brain Barrier Damage and Psychiatric Impairment in Comorbid Hepatitis C Viral Infection and Alcohol Use Disorder.
S100B and Inflammatory Cytokine Levels in Blood as Potential Markers of Blood-Brain Barrier Damage and Psychiatric Impairment in Comorbid Hepatitis C Viral Infection and Alcohol Use Disorder.
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DOI：
10.1111/acer.13796
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发表时间：
2018-06-28
期刊：
影响因子：
--
通讯作者：
Hauser P
中科院分区：
文献类型：
--
作者：
Loftis JM;Valerio J;Taylor J;Huang E;Hudson R;Taylor-Young P;Chang M;Ho SB;Dieperink E;Miranda JL;Hauser P
丙型肝炎病毒（HCV）感染和酒精使用障碍（AUD）都对免疫系统产生不利影响，导致免疫细胞信号传导和炎症过程的改变。本研究的目的是调查合并AUD如何导致HCV成人患者炎症介质异常和精神损害。在三个时间点（基线、第4周和第12周），对患有HCV的退伍军人（n = 42）和无（n = 13）合并AUD的患者的酒精使用、情绪和炎症因子进行了评估。免疫激活，血脑屏障（BBB）损伤（S100 B），肝功能和病毒载量的外周指数进行了测定，使用免疫测定和聚合酶链反应测定。共病AUD与抑郁和焦虑症状增加、肝酶水平升高和炎症因子表达改变相关。饮酒量与精神症状的严重程度呈正相关。单变量分析确定了白细胞介素（IL）-8（p = 0.006）、IL-10（p = 0.03）和S100 B（p = 0.048）的显著组间差异，AUD受试者的水平升高，尽管饮酒减少且HCV病毒载量无显著变化，但随着时间的推移，这些水平仍持续存在。对于评估的其他免疫因素，未发现研究组或时间的统计学显著性影响。探索性受试者工作特征（ROC）曲线分析评估了IL-8、IL-10和S100 B区分饮酒水平的能力，并生成了用于识别低风险和不健康饮酒组的生物标志物截止值。这些结果表明，HCV和共病AUD与更大的精神损害相关，可能是由于炎症增加、细胞因子表达失调和BBB功能受损所致。酒精诱导的血脑屏障损伤可能会增加慢性HCV感染背景下神经病理后果的风险。
Hepatitis C virus (HCV) infection and alcohol use disorder (AUD) both adversely affect the immune system resulting in alterations in immune cell signaling and inflammatory processes. The aim of this study was to investigate how co-morbid AUD contributes to abnormalities in inflammatory mediators and psychiatric impairments in adults with HCV. Alcohol use, mood, and inflammatory factors were evaluated at three time points (baseline, week 4, and week 12) in Veterans with HCV, with (n = 42) and without (n = 13) co-morbid AUD. Peripheral indices of immune activation, blood brain barrier (BBB) damage (S100B), liver function, and viral load were measured using immunoassays and polymerase chain reaction assays. Co-morbid AUD was associated with increased symptoms of depression and anxiety, elevated levels of liver enzymes, and altered expression of inflammatory factors. Alcohol consumption was positively correlated with the severity of psychiatric symptoms. Univariate analysis identified significant group differences for interleukin (IL)-8 (p = 0.006), IL-10 (p = 0.03), and S100B (p = 0.048), with increased levels in participants with AUD, which persisted over time despite reductions in alcohol use and no significant change in HCV viral load. Statistically significant effects of study group or time were not found for the other immune factors assessed. Exploratory receiver operating characteristics (ROC) curve analysis evaluated the ability of IL-8, IL-10, and S100B to differentiate between levels of alcohol consumption and generated biomarker cut-off values used to identify low risk and unhealthy alcohol use groups. These results demonstrate that HCV and co-morbid AUD is associated with greater psychiatric impairments, potentially resulting from increased inflammation, dysregulated cytokine expression, and compromised BBB function. Alcohol-induced BBB damage may increase the risk of neuropathological consequences within the context of chronic HCV infection.
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