First Author | Frank K | Year | 2020 |
Journal | PLoS One | Volume | 15 |
Issue | 12 | Pages | e0239246 |
PubMed ID | 33347446 | Mgi Jnum | J:300129 |
Mgi Id | MGI:6491368 | Doi | 10.1371/journal.pone.0239246 |
Citation | Frank K, et al. (2020) Alcohol dependence promotes systemic IFN-gamma and IL-17 responses in mice. PLoS One 15(12):e0239246 |
abstractText | 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-gamma, 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-gamma and IL-17 expression in a cell type- and organ-specific manner. Often, B cells and neutrophils were primary contributors to increased IFN-gamma and IL-17 levels while other cell types played a secondary role. We conclude that chronic alcohol exposure promotes systemic pro-inflammatory IFN-gamma 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. |