AIMS: Chronic inflammation has become increasingly recognized as a health threat for people living with HIV, given its associations with multiple diseases. Accordingly, the scientific community has prioritized the need to identify mechanisms triggering inflammation. PARTICIPANTS METHODS: A clinic-based case-control study was designed to elucidate the plausible effects of alcohol use on IL-6. Peripheral blood mononuclear cells for measuring IL-6 culture supernatant and plasma for HIV assessments were collected from 59 hazardous alcohol users and 66 nonhazardous alcohol users, who were matched according to their age, gender and US CDC HIV severity status. RESULTS: Stimulated peripheral blood mononuclear cells produced significantly higher amounts of IL-6 in hazardous alcohol users compared with nonhazardous alcohol users. However, racial status and receiving HAART significantly moderated this effect. Notably, in both HAART and non-HAART scenarios, IL-6 levels were associated with CD4 counts and viral burden. A distinctive IL-6 production pattern across racial/ethnic groups was also evident and showed that, when prescribed HAART, Hispanic hazardous alcohol users have a particularly high risk of morbidity compared with their Caucasian and African-American counterparts. After adjusting for confounders (e.g., sociodemographics and HIV disease status), regression analyses confirmed that chronic inflammation, as indicated by IL-6 levels (log), is associated with alcohol use, race/ethnicity and thrombocytopenia, and tended to be related to concurrent smoking. CONCLUSION: Our data confirm that, despite HAART, people living with HIV still have a persistent inflammatory response that, in our study, was associated with chronic hazardous alcohol use. The data also highlight racial/ethnic disparities in IL-6 that justify further investigations.
AIMS: Chronic inflammation has become increasingly recognized as a health threat for people living with HIV, given its associations with multiple diseases. Accordingly, the scientific community has prioritized the need to identify mechanisms triggering inflammation. PARTICIPANTS METHODS: A clinic-based case-control study was designed to elucidate the plausible effects of alcohol use on IL-6. Peripheral blood mononuclear cells for measuring IL-6 culture supernatant and plasma for HIV assessments were collected from 59 hazardous alcohol users and 66 nonhazardous alcohol users, who were matched according to their age, gender and US CDC HIV severity status. RESULTS: Stimulated peripheral blood mononuclear cells produced significantly higher amounts of IL-6 in hazardous alcohol users compared with nonhazardous alcohol users. However, racial status and receiving HAART significantly moderated this effect. Notably, in both HAART and non-HAART scenarios, IL-6 levels were associated with CD4 counts and viral burden. A distinctive IL-6 production pattern across racial/ethnic groups was also evident and showed that, when prescribed HAART, Hispanic hazardous alcohol users have a particularly high risk of morbidity compared with their Caucasian and African-American counterparts. After adjusting for confounders (e.g., sociodemographics and HIV disease status), regression analyses confirmed that chronic inflammation, as indicated by IL-6 levels (log), is associated with alcohol use, race/ethnicity and thrombocytopenia, and tended to be related to concurrent smoking. CONCLUSION: Our data confirm that, despite HAART, people living with HIV still have a persistent inflammatory response that, in our study, was associated with chronic hazardous alcohol use. The data also highlight racial/ethnic disparities in IL-6 that justify further investigations.
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