Inflammation and infection in human cocaine addiction

Ersche, Karen D.; Döffinger, Rainer

doi:10.1016/j.cobeha.2016.12.007

Cited by 24 publications

(31 citation statements)

References 50 publications

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“…In addicted individuals, overall results concerning number and percentage of such cells are still inconsistent. For instance, elevated percentage of T CD4 + cells were observed in individuals with cocaine use (52, 53), corroborating our findings; however, other studies did not find such association (15). In addition, alcohol exposure was related to a decline in total T CD4 + cells (54).…”

Section: Discussionsupporting

confidence: 91%

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Cocaine Use Disorder Is Associated With Changes in Th1/Th2/Th17 Cytokines and Lymphocytes Subsets

et al. 2019

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Background: Cocaine is a psychostimulant drug with high addictive proprieties. Evidence suggests that cocaine use leads to critical changes in the immune system, with significant effects on T, B, and natural killer (NK) cells and influencing peripheral levels of cytokines. The presence of abstinence-related symptoms during detoxification treatment is known to influence the prognosis. Here, our aim was to investigate immune profiles in women with cocaine use disorder (CUD) according to withdrawal symptoms severity.Methods: Blood samples and clinical data were collected at onset of detoxification treatment of 50 women with CUD. The patients were stratified according to Cocaine Selective Severity Assessment (CSSA) scores in low withdrawal (L-W) and high withdrawal (H-W) categories. In addition, we also included a control group with 19 healthy women as reference to immune parameters. Peripheral blood was collected and lymphocyte subsets were phenotyped by multi-color flow cytometry (B cells, CD4+ T, CD8+ T, NK cells, and different stages of T-cell differentiation). PBMCs from patients and healthy controls were stimulated in vitro with phytohemagglutinin (1%) for 72 h to assess the production of Th1/Th2/Th17 cytokines.Results: Following stimulation, lymphocytes from women with CUD produced increased levels of Th1/Th2/Th17 cytokines. However, higher levels of IL-2 and IL-17 were observed only in the L-W group, while higher levels of IL-6 were detected in the H-W group compared to controls. H-W group showed lower percentage of early-differentiated Th cells (CD4+CD27+CD28+), elevated percentage of Th cells (CD3+CD4+), intermediate-differentiated Th cells (CD4+CD27−CD28+), and B cells (CD3−CD19+). Both CUD groups showed decreased percentages of naïve T cells (CD3+CD4+CD45RA+ and CD3+CD8+CD45RA+).Conclusion: Our data demonstrated that CUD can lead to increased production of Th1/Th2/Th17 cytokines and lymphocyte changes.

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Section: Discussionsupporting

confidence: 91%

“…Regarding NK cells, data remains inconsistent. We did not observe any alteration in NK cell population, as Ruiz et al (57) in contrast, other studies with cocaine users even detected an increase (15, 56) as well as a decrease in NK cells (50, 52).…”

Section: Discussioncontrasting

confidence: 64%

Cocaine Use Disorder Is Associated With Changes in Th1/Th2/Th17 Cytokines and Lymphocytes Subsets

et al. 2019

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“…Cocaine has multiple extracranial systemic eff ects due to its vasoconstrictive, prothrombotic, endotheliotoxic and arrhythmogenic properties, potentially aff ecting every organ in the human body, including vascular endothelium, immune and endocrine systems [1,2,8,9,10,11,12,13,14,15] Cocaine and its derivates and metabolites can affect the kidney, causing both acute and chronic renal injury (table 1). The major underlying mechanisms include: renal ischemia due to vasoconstriction and activation of thrombogenesis, endothelial toxicity and vasculitis, rhabdomyolysis, tubulo-interstitial toxicity, stimulation of mesangial matrix synthesis and mesangial cell proliferation and fi brogenesis, inhibition of macrophageal IL-6 and IL-8 synthesis, changes in T-and B-cell immune response, development of infection-associated amyloidosis [8,9,10,12,13]. Moreover, cocaine exposure in utero may lead to urogenital, cardiovascular, nervous system and other abnormalities [11,12,14,15].…”

Section: Nikolova 1 Vl Milenova 1 D Yosifov 1 Y Vlahov 2 mentioning

confidence: 99%

“…Sympathic activation with subsequent vasoconstriction (due to suppression of nitric oxide-mediated vasodilation); Changes in endothelial function with increased production of endothelin and decreased synthesis of NO by the endothelial cells -both due to direct effects upon the endothelium and changes in cytokine levels (i.e., inhibition of IL-8 and IL-6 secretion with subsequent stimulation of TGF-beta secretion); Development of procoagulant state due to platelet activation; Inhibition of prostaglandin E2 and I2 (prostacyclin) secretion with subsequent vasoconstriction and platelet activation;5. Generation of reactive oxygen species as by-products of cocaine degradation and inhibition of mitochondrial respiration, decrease of gluthatione levels and oxidation-mediated cell death.Moreover, cocaine can alter immune function[13] due to the presence of dopamine-mediated alterations in B-, T-and NK-cell function, triggered by cocaine.…”

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confidence: 99%

Renal Changes in Cocaine Abuse and Addiction

Nikolova

Milenova

Yosifov

et al. 2019

Acta Medica Bulgarica

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Cocaine is a natural alkaloid extracted from the leaves of the South American plant Erythroxylum coca or synthesized chemically. After cannabis, it is the second most frequently abused recreational substance worldwide. Cocaine can affect every tissue and organ within the human body, including the kidneys, causing tissue ischemia due to vasoconstriction, endothelial dysfunction and damage, procoagulant activity and oxidative stress with subsequent ischemic infarctions and fibrosis. The renal changes in cocaine abuse and addiction are due to rhabdomyolysis, ischemic, hypertensive, and inflammatory changes with the development of cell proliferation and fibrosis. The authors present three patients with cocaine-associated renal damage and discuss the underlying mechanisms of cocaine-induces tissue changes.

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“…These neuroadaptations likely result from the proinflammatory effects of cocaine on the central nervous system, including increased oxidative stress, induction of inflammatory cytokines, and greater permeability of the blood-brain-barrier (Buch et al, 2012). It has been proposed that dopamine dysregulation acts as a catalyst for dysfunctional immune regulation that underlies these neuroinflammatory responses (Ersche & Döffinger, 2017). Cocaine-induced neuroadaptations that affect reward processing and decision-making may lead to riskier decisions (Heil, Johnson, Higgins, & Bickel, 2006;Rosselli, Ardila, Lubomski, Murray, & King, 2001;Verdejo-Garcia, Perales, & Perez-Garcia, 2007).…”

Section: Introductionmentioning

confidence: 99%

Neural sensitivity to risk in adults with co-occurring HIV infection and cocaine use disorder

Bell

Towe

Lalee

et al. 2020

Cogn Affect Behav Neurosci

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Persons with co-occurring HIV infection and cocaine use disorder tend to engage in riskier decision-making. However, the neural correlates of sensitivity to risk are not well-characterized in this population. The purpose of this study was to examine the neural interaction effects of HIV infection and cocaine use disorder to sensitivity to risk. The sample included 79 adults who differed on HIV status and cocaine use disorder. During functional magnetic resonance imaging (fMRI), participants completed a Wheel of Fortune (WoF) task that assessed neural activation in response to variations of monetary risk (i.e., lower probability of winning a larger reward). Across groups, neural activation to increasing risk was in cortical and subcortical regions similar to previous investigations using the WoF in nondrug-using populations. Our analyses showed that there was a synergistic effect between HIV infection and cocaine use in the left precuneus/posterior cingulate cortex and hippocampus, and right postcentral gyrus, lateral occipital cortex, cerebellum, and posterior parietal cortex. HIV+ individuals with cocaine use disorder displayed neural hyperactivation to increasing risk that was not observed in the other groups. These results support a synergistic effect of co-occurring HIV infection and cocaine dependence in neural processing of risk probability that may reflect compensation. Future studies can further investigate and validate how neural activation to increasing risk is associated with risk-taking behavior.

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Inflammation and infection in human cocaine addiction

Cited by 24 publications

References 50 publications

Cocaine Use Disorder Is Associated With Changes in Th1/Th2/Th17 Cytokines and Lymphocytes Subsets

Cocaine Use Disorder Is Associated With Changes in Th1/Th2/Th17 Cytokines and Lymphocytes Subsets

Renal Changes in Cocaine Abuse and Addiction

Neural sensitivity to risk in adults with co-occurring HIV infection and cocaine use disorder

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