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Published on: February 6, 2019
Cytokine Networks in Alcohol Use Disorder: A Narrative Review Highlighting Research Gaps and Future Priorities
Carmen M Galvez-Sánchez1,2, Julio A Camacho-Ruiz1,3, Cristina González-Lara4
1Department of Personality, Evaluation and Psychological Treatment, Faculty of Psychology and Speech Therapy, University of Murcia, Building 31, 30100 Murcia, Spain.
Alcohol Use Disorder (AUD) involves immune system changes, with elevated pro-inflammatory cytokines like IL-6 and TNF-α during use and early abstinence. Sustained abstinence may normalize these markers, but severe AUD can cause lasting immune dysregulation.
Area of Science:
- Neuroimmunology
- Psychiatry
- Public Health
Background:
- Alcohol Use Disorder (AUD) is a major public health issue linked to cognitive deficits and immune dysfunction.
- Neuroimmune signaling, involving microglial activation and cytokines, is implicated in AUD development and relapse.
- Cytokines and interleukins (ILs) play a critical role in AUD pathophysiology.
Purpose of the Study:
- To review and synthesize current evidence on the role of cytokines and interleukins in AUD.
- To examine how alcohol exposure, withdrawal, and abstinence modulate these immune markers.
- To identify potential biomarkers and therapeutic targets for AUD.
Main Methods:
- A comprehensive narrative review of studies on cytokine and interleukin profiles in adults with AUD.
- Searches conducted in PubMed, Scopus, and Web of Science databases.
- Synthesis of findings to identify patterns, inconsistencies, and research gaps.
Main Results:
- AUD is associated with altered cytokine profiles, including elevated pro-inflammatory markers (IL-1β, IL-6, TNF-α, IL-8, IL-18) during use and early abstinence.
- Anti-inflammatory marker IL-10 shows fluctuating levels; immune changes correlate with systemic inflammation, neurotoxicity, and AUD severity.
- Cytokine levels may normalize with sustained abstinence, but severe AUD can lead to persistent immune dysregulation; associations with anxiety and depression noted.
Conclusions:
- Immune dysregulation and altered cytokine profiles are central to AUD pathophysiology.
- Cytokines may serve as potential biomarkers for AUD progression and treatment response.
- Future research should focus on longitudinal studies, diverse populations, and mechanistic investigations for targeted immunomodulatory therapies.
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