Aberrations in peripheral inflammatory cytokine levels in substance use disorders: a meta‐analysis of 74 studies

Abstract

Aims To characterize the peripheral inflammatory cytokine profile in people with substance use disorders (SUDs). Design Systematic review and meta‐analysis. Setting Clinical studies that evaluated peripheral blood inflammatory cytokine levels in patients with SUDs and healthy controls Participants SUD patients and healthy controls. Measurements PubMed and Web of Science were systematically searched for relevant studies. Two investigators independently selected studies and extracted data. A total of 77 articles were included in the meta‐analysis, containing 5649 patients with SUDs and 4643 healthy controls. Data were pooled using a random‐effects model by the Comprehensive Meta‐Analysis version 2 software. Findings Concentrations of interleukin (IL)‐6) in 32 studies, tumor necrosis factor (TNF)‐α in 28 studies, IL‐10 in 20 studies, IL‐8 in 17 studies, C‐reactive protein in 14 studies, IL‐4 in 10 studies, IL‐12 in seven studies, monocyte chemoattractant protein (MCP)‐1 in 6 studies, TNF‐receptor 2 (TNF‐R2) in four studies and granulocyte–macrophage colony‐stimulating factor (GM‐CSF) in three studies were significantly higher in patients with SUDs compared with healthy controls, while concentrations of leptin in 14 studies were significantly lower in patients with SUDs compared with healthy controls. The findings were inconclusive for the associations between interferon‐γ, IL‐1β, IL‐2, IL‐1 receptor antagonist (IL‐1RA), transforming growth factor (TGF)‐β1, G‐CSF, C‐C motif chemokine 11, TGF‐α and SUDs. Conclusions People with substance use disorders (SUDs) appear to have higher peripheral concentrations of IL‐4, IL‐6, IL‐8, IL‐10, IL‐12, TNF‐α, C‐reactive protein, MCP‐1, TNF‐R2 and GM‐CSF and lower peripheral concentrations of leptin than people without SUDs. This strengthens the view that SUD is accompanied by an inflammatory response.

COVID-19 risk, course and outcome in people with mental disorders: a systematic review and meta-analyses

“…This may result in late detection and, with that, delayed medical care. Moreover, in this group, too, compromised immune functioning and poor physical fitness probably contribute (Beurel et al, 2020;Chireh et al, 2019;Wei et al, 2020).…”

Plasma Concentrations of Neurofilament Light Chain Protein and Brain-Derived Neurotrophic Factor as Consistent Biomarkers of Cognitive Impairment in Alcohol Use Disorder

“…The explanation of why these biomarkers are insufficient in this population could be due to the influence of additional factors in cognitive dysfunction, such as other nutritional deficiencies (i.e., low BMI, ascorbic acid deficiency, or thiamine deficiency) [ 17 , 18 ], comorbid psychiatric disorders (i.e., affective disorders) [ 19 ], as well as inflammation and oxidative stress caused by chronic alcohol intake or alcohol withdrawal episodes per se [ 20 ]. Heavy alcohol consumption throughout life triggers a proinflammatory organic state that leads to neurocognitive alterations [ 21 , 22 , 23 ]. Alcohol can stimulate Toll-like receptor 4 (TLR4), which activates several signaling pathways (i.e., Nuclear Factor-κB, inducible Nitric Oxide Synthase), resulting in the release of cytokines, chemokines, and oxidative–nitrosative stress [ 24 , 25 , 26 ], associated with neuroinflammation and structural brain damage [ 27 , 28 , 29 ].…”

Vascular Endothelial Growth Factor as a Potential Biomarker of Neuroinflammation and Frontal Cognitive Impairment in Patients with Alcohol Use Disorder

“…Furthermore, chemokine decompensation described in plasma, serum and cerebrospinal fluid has been associated with several psychiatric and neurodegenerative diseases such as mild cognitive impairment, Alzheimer's disease, Parkinson's disease, schizophrenia, bipolar disorder and major depression [27][28][29][30]. However, despite the interaction between alcohol and immunological mediators having been well investigated [31,32], little is known about whether these immunoinflammatory signals impact the development of AUD-associated cognitive impairment. Long-lasting brain induction of the proinflammatory cytokines tumor necrosis factor alpha (TNFα), interleukin (IL)-1β and monocyte chemoattractant protein-1 (MCP-1) and the anti-inflammatory cytokine IL-10 have been related to microglial activation and reduced neurogenesis in mice exposed to LPS endotoxin after ethanol treatment [33].…”