期刊
JCI INSIGHT
卷 5, 期 3, 页码 -出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/jci.insight.131277
关键词
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资金
- NIH [R01 DK101737-01A1, U01 AA022614-01A1, R01 DK099205-01A1, P50AA011999, AI043477, NS093055, NS054734, R01 CA 100660, R01 AA020864, R21AA024935, R01 DK107682, R01 AA025208, R21 AA024198, P60 AA006420, R01 AA021491]
- Herman Lopata Memorial Hepatitis Postdoctoral ALF Fellowship
- Veterans Affairs Research and Administration [1I01CX000361]
- US Department of Defense [W81XWH-12-1-0497]
- Showalter Scholar Award from the Ralph W. and Grace M. Showalter Research Trust
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [ZIAAA000369] Funding Source: NIH RePORTER
Chronic alcohol abuse has a detrimental effect on the brain and liver. There is no effective treatment for these patients, and the mechanism underlying alcohol addiction and consequent alcohol-induced damage of the liver/brain axis remains unresolved. We compared experimental models of alcoholic liver disease (ALD) and alcohol dependence in mice and demonstrated that genetic ablation of IL-17 receptor A (IL-17ra(-/-)) or pharmacological blockade of IL-17 signaling effectively suppressed the increased voluntary alcohol drinking in alcohol-dependent mice and blocked alcohol-induced hepatocellular and neurological damage. The level of circulating IL-17A positively correlated with the alcohol use in excessive drinkers and was further increased in patients with ALD as compared with healthy individuals. Our data suggest that IL-17A is a common mediator of excessive alcohol consumption and alcohol-induced liver/brain injury, and targeting IL-17A may provide a novel strategy for treatment of alcohol-induced pathology.
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