Modulation of salivary cytokines in response to alcohol, tobacco and caffeine consumption: a pilot study

Abstract

It has been shown that long-term stimulant consumption alters the biological and microbiological status of the oral cavity. We present a pilot study describing stimulant-specific oral immunomodulation in the oral cavity. Changes in salivary cytokine levels in response to long-term alcohol, tobacco and caffeine were identified. Volunteers were recruited from amongst the patients visiting University Dental Clinic of CEU Cardenal Herrera University (Alfara del Patriarca, Spain). Participants were grouped according to their self-reported levels of consumption of either caffeine, alcohol or tobacco (control group volunteers were non-consumers of all three). Informed consent was provided and stimulated saliva samples were obtained and assayed for interleukin-1α IL-1α), Tumor Necrosis Factor α (TNF-α) and Interferon γ IFN-γ). Long-term, high-level consumers of alcohol or tobacco exhibited elevated salivary concentrations of the three inflammatory cytokines with respect to control values. Specifically, IL-1α was found to be elevated in alcohol users whilst IFN-γ concentration higher in tobacco users versus controls. Long-term caffeine consumers displayed elevated levels of IFN-γ and TNF-α, whereas IL-1α levels were reduced with respect to control volunteers. This pilot study demonstrates that salivary cytokines can be modulated in response to quantity and duration of alcohol, caffeine or tobacco consumption.

Inflammatory Biomarkers, Microbiome, Depression, and Executive Dysfunction in Alcohol Users

“…To the best of our knowledge, data from the current study provides new evidence identifying potential salivary biomarkers associated with alcohol use. The inflammatory profile revealed in the AG is different from other studies reporting that increases in serum/plasma TNF-α, IL-1, IL-6, IL-12, IL1-β, and IL-8 are associated with chronic alcohol consumption or alcohol-related liver diseases [16,101,102]. This difference might be due to genetics, age, cultural, and behavioral aspects (e.g., diet and lifestyle) [103].…”

Can smoking alter salivary homeostasis? A systematic review on the effects of traditional and electronic cigarettes on qualitative and quantitative saliva parameters

“…In smokers, macrophages produce more TNF-α, IL-1 and IL-6 than in non-smokers. 142 In addition to changes in macrophage morphology (e.g., cytoplasm thickening and its higher density), these cells also show higher CD14 expression, stronger inhibition of lymphocyte and NK (natural killer) proliferation, and less ability to phagocytose microorganisms. Cigarette smoke also changes the T helper (Th)1/Th2 cell ratio.…”

Purine-Induced IFN-γ Promotes Uric Acid Production by Upregulating Xanthine Oxidoreductase Expression

“…In addition, high purine and purine derivative intake not only increases serum UA, but also associated with physiological inflammatory/anti-inflammatory activity (16)(17)(18). Long-term, high-level caffeine (whose main metabolite is paraxanthine) consumers often have elevated levels of IFN-g and TNF-a (19). The upregulation of XOR expression, by cytokines IL-1, IL-6 and IFN-g, has been reported in lung, renal, and mammary epithelial cells (20)(21)(22)(23), but their effect on XOR expression and UA production in hepatocytes remained unknown.…”