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Increase in plasma CCL11 (Eotaxin-1) in patients with alcohol dependence and changes during detoxification
Ming-Chyi Huang1, Ren-Hua Chung2, Pei-Hsuan Lin3
1Department of Psychiatry, Taipei City Psychiatric Center, Taipei City Hospital, Taipei, Taiwan; Department of Psychiatry, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Psychiatric Research Center, Taipei Medical University Hospital, Taipei 110, Taiwan.
Background:
Alcohol is known to modulate the immune system. Neuroinflammatory cytokine dysregulation plays an essential role in the pathophysiology of alcohol dependence (AD). Preclinical studies have indicated that alcohol consumption upregulates the pro-inflammatory cytokine CC motif ligand 11 (CCL11, also known as eotaxin-1). We examined CCL11 levels in patients with AD and in mice administered alcohol.
Methods:
The plasma CCL11 levels of 151 patients with AD and 116 healthy controls were measured. In addition, we followed the CCL11 levels, alcohol cravings and psychological symptoms in patients with AD after 1 and 2 weeks of detoxification. Furthermore, we examined CCL11 changes in mice administered alcohol for 5 days.
Results:
CCL11 levels were higher in patients with AD than in controls and declined during detoxification. CCL11 levels were positively correlated with AD severity (p < 0.001). Furthermore, mice exposed to alcohol exhibited a higher CCL11 level. The receiver operating characteristic curve revealed that a CCL11 level of 72.5 pg/mL could significantly differentiate patients with AD from controls (area under the curve: 0.77; p < 0.001). Reductions in CCL11 levels during detoxification were correlated with reductions in alcohol craving, depression, and anxiety.
Conclusions:
Our data from humans and mice suggest that chronic alcohol consumption is associated with an increase in CCL11 levels. CCL11 levels are correlated with AD severity and may be a potential indicator of AD. The CCL11 reduction after alcohol discontinuation is associated with alleviation of clinical symptoms. Collectively, our findings suggest that CCL11 is involved in the neurobiological mechanisms underlying AD.
