Reduced Serum Levels of Cluster of Differentiation 200 in Alcohol-Dependent Patients.

AIM: Chronic alcohol consumption can activate and dysregulate the neuroimmune system which leads to neuroinflammation. Neuroimmune regulatory proteins (NIReg) (e.g. Cluster of Differentiation 200 (CD200)) are the regulators of innate immune response and are responsible for silencing the innate immunity and suppression of inflammation. In this study, we explored the changes of serum levels of CD200 in patients with alcohol dependence at baseline, after one-week alcohol withdrawal and after one-month of alcohol abstinence. METHODS: Seventeen patients with alcohol dependence admitted for de-addiction treatment and 12 healthy controls were enrolled in the study. Blood samples were collected at baseline, after one-week, and after one-month, and CD200 levels were measured using enzyme-linked immunosorbent assay kit and compared with the healthy controls. RESULTS: The serum level of the neuroimmune regulatory protein CD200 in alcohol dependent group (at baseline) was significantly lower compared to healthy controls (p=0.003), and increased after one-week, and one-month period. CONCLUSION: The present study indicates that decrease of CD200 serum levels in alcohol dependent patients and its rise during alcohol withdrawal and abstinence may provide a preliminary evidence of the role of neuroimmune regulatory proteins in neuroadaptation during alcohol withdrawal.

Decreased expression of CD200 on peripheral blood leukocytes in alcohol dependence.

Chronic alcohol use induces innate immune genes, which activate the innate immune system. Neuroimmune regulatory proteins [e.g., Cluster of Differentiation 200 (CD200)] are immune response regulators and are involved in balancing the immune response. This study aimed to investigate the expression of CD200 on the surface of peripheral blood leukocytes in patients with alcohol use disorder and compare them with controls. Fifty male patients with alcohol use disorder were included in the study. A baseline assessment was done, and alcohol use history, craving, and withdrawal scores were collected. A 2-mL venous blood sample was collected from cases and controls for immunophenotyping of CD200. The control group consisted of 50 participants with similar socio-economic backgrounds. The cellular expression of CD200 on total leukocytes (median ± IQR) [39.94 (28.85, 50.01)] in cases was significantly lower compared to controls [45.07 (37.70, 51.69)] (U = 896, p = 0.015). Expression of CD200 on lymphocytes in cases was negatively correlated with years of heavy drinking and this was statistically significant (r = -0.321, p = 0.023). The study indicates that cellular expression of CD200 on the surface of peripheral blood leukocytes is reduced in alcohol-dependent patients. This reduction can contribute to exaggerated immune activity, release of pro-inflammatory cytokines, chronic microglial activation, neuroinflammation, and neurodegeneration in alcohol dependence.