Jennifer M Loftis1,2, Juno Valerio1, Jonathan Taylor1,2, Elaine Huang1,2, Rebekah Hudson1, Patricia Taylor-Young3,4, Michael Chang5,6, Samuel B Ho7,8, Eric Dieperink9,10, Juan Luis Miranda11, Peter Hauser11,12,13. 1. Research & Development Service , VA Portland Health Care System, Portland, Oregon. 2. Department of Psychiatry , Oregon Health & Science University, Portland, Oregon. 3. Nursing Research Department , VA Portland Health Care System, Portland, Oregon. 4. School of Nursing , Oregon Health & Science University, Portland, Oregon. 5. Gastroenterology , VA Portland Health Care System, Portland, Oregon. 6. Internal Medicine , Oregon Health & Science University, Portland, Oregon. 7. VA San Diego Healthcare System , San Diego, California. 8. Department of Medicine , University of California San Diego, San Diego, California. 9. Minneapolis VA Healthcare System , Minneapolis, Minnesota. 10. Department of Psychiatry , University of Minnesota School of Medicine, Minneapolis, Minnesota. 11. VA Long Beach Health Care System , Long Beach, California. 12. Department of Psychiatry and Human Behavior , University of California-Irvine, Irvine, California. 13. Department of Psychiatry , University of California San Diego, San Diego, California.
Abstract
BACKGROUND: 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 comorbid AUD contributes to abnormalities in inflammatory mediators and psychiatric impairments in adults with HCV. METHODS: Alcohol use, mood, and inflammatory factors were evaluated at 3 time points (baseline, week 4, and week 12) in Veterans with HCV, with (n = 42) and without (n = 13) comorbid AUD. Peripheral indices of immune activation, blood-brain barrier (BBB) damage (S100 calcium-binding protein B [S100B]), liver function, and viral load were measured using immunoassays and polymerase chain reaction assays. RESULTS: Comorbid 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 in 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 characteristic curve analysis evaluated the ability of IL-8, IL-10, and S100B to differentiate between levels of alcohol consumption and generated biomarker cutoff values used to identify low risk and unhealthy alcohol use groups. CONCLUSIONS: These results demonstrate that HCV and comorbid AUD are 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. Published 2018. This article is a U.S. Government work and is in the public domain in the USA.
BACKGROUND: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 comorbid AUD contributes to abnormalities in inflammatory mediators and psychiatric impairments in adults with HCV. METHODS:Alcohol use, mood, and inflammatory factors were evaluated at 3 time points (baseline, week 4, and week 12) in Veterans with HCV, with (n = 42) and without (n = 13) comorbid AUD. Peripheral indices of immune activation, blood-brain barrier (BBB) damage (S100 calcium-binding protein B [S100B]), liver function, and viral load were measured using immunoassays and polymerase chain reaction assays. RESULTS: Comorbid 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 in 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 characteristic curve analysis evaluated the ability of IL-8, IL-10, and S100B to differentiate between levels of alcohol consumption and generated biomarker cutoff values used to identify low risk and unhealthy alcohol use groups. CONCLUSIONS: These results demonstrate that HCV and comorbid AUD are 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. Published 2018. This article is a U.S. Government work and is in the public domain in the USA.
Entities:
Keywords:
Alcohol Use Disorders; Blood-Brain Barrier; Cytokines; Depression; Hepatitis C
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