Alcohol use predicts elevation in inflammatory marker soluble CD14 in men living with HIV

ABSTRACT

Independently, HIV infection and heavy alcohol use increase microbial translocation (MT) of gut products into systemic circulation. MT and consequent immune response have been linked to chronic inflammation and a host of negative health outcomes in individuals living with HIV. However, previous research has not systematically investigated the immune correlates of heavy drinking specifically within the HIV-positive population. This pilot study investigated MT and immune activation as a function of alcohol use in 21 HIV-positive men who met NIAAA criteria for heavy drinking. Participants averaged 46.7 ± 8.5 (mean ± standard deviation) years of age, 12.2 ± 9.2 years since HIV diagnosis, 337 ± 158 CD4 nadir, and 643 ± 245 current CD4 count. All participants were virologically suppressed on antiretroviral therapy. Data on alcohol use and immune function were collected at baseline and three-month follow-up. Plasma concentrations of markers of MT and immune activation (lipopolysaccharide (LPS), soluble CD14 (sCD14), endotoxin core antibody immunoglobulin M (EndoCAb)) were measured using enzyme-linked immunosorbent assays. Generalized estimating equation models tested alcohol use variables as predictors of LPS, sCD14, and EndoCAb levels. Greater quantity and frequency of drinking significantly predicted higher sCD14 levels (p’s < .01). Conversely, longer duration of abstinence from alcohol significantly predicted lower sCD14 levels (p < .001). These results remained significant after controlling for age, HIV duration, smoking status, current CD4 count, CD4 nadir, and antiretroviral drug type. In addition, participants with ≥50% relative reduction in drinks per week showed a significant decrease (p < .05) in sCD14 from baseline to three-month follow-up. This pilot study provides preliminary evidence that heavy drinking may increase a key inflammatory marker in HIV-infected individuals with suppressed infection.

KEYWORDS:

• sCD14
• alcohol
• heavy drinking
• microbial translocation
• HIV infection
• inflammation

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development [grant number K24HD080539] (PI: Ramratnam); by the Retrovirology Core of the Lifespan Tufts Brown CFAR [grant number P30AI042853]; by the National Institute on Alcohol Abuse and Alcoholism [grant number P01AA019072] (PI: Monti), [grant number K05AA019681] (PI: Monti), and [grant number T32AA007459] (PI: Monti); and by the National Institute of Nursing Research [grant number K23NR014951] (PI: Cioe).