Substantial evidence supports the view that inflammatory processes contribute to brain alterations in HIV infection. Mechanisms recently proposed to underlie neuropathology in Alcohol Use Disorder (AUD) include elevations in peripheral cytokines that sensitize the brain to the damaging effects of alcohol. This study included 4 groups: healthy controls, individuals with AUD (abstinent from alcohol at examination), those infected with HIV, and those comorbid for HIV and AUD. The aim was to determine whether inflammatory cytokines are elevated in AUD as they are in HIV infection. Cytokines showing group differences included interferon gammainduced protein 10 (IP-10) and tumor necrosis factor α (TNFα). Follow-up t-tests revealed that TNFα and IP-10 were higher in AUD than controls but only in AUD patients who were seropositive for Hepatitis C virus (HCV). Specificity of TNFα and IP10 elevations to HCV infection status was provided by correlations between cytokine levels and HCV viral load and indices of liver integrity including albumin/globulin ratio, fibrosis scores, and AST/platelet count ratio. Because TNFα levels were mediated by HCV infection, this study provides no evidence for elevations in peripheral cytokines in "uncomplicated", abstinent alcoholics, independent of liver disease or HCV infection. Nonetheless, these results corroborate evidence for elevations in IP-10 and TNFα in HIV and for IP-10 levels in HIV+HCV coinfection.
Zahr cytokines in pg-per-ml
These are the raw, pg/mL data from the shortly to be published PlosOne paper: Peripheral TNFα elevations in Alcohol Use Disorders are associated with Hepatitis C Infection, Natalie M. Zahr, Priya Asok, Edith V. Sullivan, & Adolf Pfefferbaum. Based on the recommendations of the Human Immune Monitoring Center (HIMC), http://iti.stanford.edu/himc.html, we used mean florescence intensity (MFI) in the manuscript. However, here we release the pg/mL data as that seems to be more useful for general use. Whole blood samples (n=223), collected in lavender EDTA tubes between March 2013 and October 2016 were centrifuged (500 rcf at room temperature for 10min). Plasma was transferred to 1.5mL conical tubes, centrifuged at 13,000 rcf at room temperature for another 10min, and the resulting supernatant was transferred to 1.5mL conical tubes for storage at −80° C until analysis by the HIMC. The HIMC, which continually benchmarks processes to minimize technical variability (Maecker et al., 2005), performed immunological assays. Human 41-plex kits (HCYTOMAG-60K, 7 kits, each able to run 42 samples) were purchased from EMD Millipore and used according to the manufacturer’s recommendations with modifications as described. Briefly, samples were mixed with antibody-linked magnetic beads on a 96-well plate and incubated overnight incubation at 4°C with shaking. Cold and Room temperature incubation steps were performed on an orbital shaker at 500-600 rpm. Plates were washed twice with wash buffer in a Biotek ELx405 washer. Following one hour incubation at room temperature with biotinylated detection antibody, streptavidin fluorochrome (i.e., streptavidin-PE) was added for 30 minutes with shaking. Plates were washed as above and PBS added to wells for reading in the Luminex 200 Instrument with a lower bound of 50-100 beads per sample per cytokine. Each sample was measured in duplicate. Custom assay control beads by Radix Biosolutions were added to all wells.
Zahr_cytokines in pg-per-ml.csv
