Abstract
Alcohol use disorder (AUD) is a chronic relapsing disorder characterized by an impaired ability to stop or control alcohol use despite adverse social, occupational, or health consequences. AUD is associated with a variety of physiological changes and is a substantial risk factor for numerous diseases. We aimed to characterize systemic alterations in immune responses using a well-established mouse model of chronic intermittent alcohol exposure to induce alcohol dependence. We exposed mice to chronic intermittent ethanol vapor for 4 weeks and analyzed the expression of cytokines IFN-γ, IL-4, IL-10, IL-12 and IL-17 by different immune cells in the blood, spleen and liver of alcohol dependent and non-dependent control mice through multiparametric flow cytometry. We found increases in IFN-γ and IL-17 expression in a cell type- and organ-specific manner. Often, B cells and neutrophils were primary contributors to increased IFN-γ and IL-17 levels while other cell types played a secondary role. We conclude that chronic alcohol exposure promotes systemic pro-inflammatory IFN-γ and IL-17 responses in mice. These responses are likely important in the development of alcohol-related diseases, but further characterization is necessary to understand the initiation and effects of systemic inflammatory responses to chronic alcohol exposure.
Highlights
Chronic intermittent alcohol exposure is associated with increased risk of cancer, organ damage, and infection [1,2,3]
Chronic alcohol alters inflammatory processes which regulate immune function. This is often characterized by changes in cytokine expression and immune defense mechanisms of type 1—cell-mediated immunity associated with IFN-γ, IL-12 and TNF-α expression—or type 2—humoral immunity associated with IL-4, interleukin 10 (IL10) and IgE expression—immune responses [4]
One mechanism through which chronic alcohol exposure leads to adverse clinical outcomes is well characterized: increased expression of TNF-α by liver macrophages promotes inflammation leading to alcoholic liver disease (ALD) development in human alcoholics [5,6]
Summary
Chronic intermittent alcohol exposure is associated with increased risk of cancer, organ damage, and infection [1,2,3]. Chronic alcohol alters inflammatory processes which regulate immune function. This is often characterized by changes in cytokine expression and immune defense mechanisms of type 1—cell-mediated immunity associated with IFN-γ, IL-12 and TNF-α expression—or type 2—humoral immunity associated with IL-4, IL10 and IgE expression—immune responses [4]. One mechanism through which chronic alcohol exposure leads to adverse clinical outcomes is well characterized: increased expression of TNF-α by liver macrophages promotes inflammation leading to alcoholic liver disease (ALD) development in human alcoholics [5,6].
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