Inflammatory cytokines in alcohol use disorder patients are lower in smokers and users of smokeless tobacco.

Abstract

Smoking and alcohol use often cooccur, and the use of nicotine-containing products is particularly common among persons with alcohol use disorder (AUD). Recent evidence shows that chronic alcohol use leads to inflammation through increased gut permeability and dysregulated cytokine levels. While cigarette smoking also has detrimental health effects, nicotine is indicated to exert immune dampening effects in some settings. Preclinical evidence demonstrates that nicotine may dampen alcohol induced inflammation, but inflammatory responses after use of nicotine has not yet been studied in persons with AUD. The current study compared the level of circulating cytokines in non-tobacco users, smokers, users of Swedish snus and dual tobacco users among abstinent AUD inpatients. We collected blood samples and information about somatic and mental health, and tobacco habits from 111 patients in residential treatment for AUD and 69 healthy controls. Levels of interferon (IFN)-γ, interleukin (IL)-10, tumor necrosis factor (TNF)-α, IL-17a, IL-1β, IL-6, IL-8, IL-1 receptor antagonist (ra), and monocyte chemoattractant protein (MCP)-1 were examined using a multiplex assay. Patients with AUD had higher levels of seven cytokines compared to healthy controls. Among the AUD patients, nicotine users had lower levels of IL-10, TNF-α, IL-17a, IL-1β, IL-8, and MCP-1 (all p<0.05). Our findings may indicate that nicotine has anti-inflammatory effects in patients with AUD. Still nicotine use cannot be recommended as a viable therapeutic option to reduce alcohol-induced inflammation because it may cause other adverse effects. Future studies of cytokine patterns in relation to mental or somatic health conditions are warranted to carefully investigate the effect of nicotine, by monitoring the use of any tobacco or nicotine product.