Methamphetamine-induced alterations in intestinal mucosal barrier function occur via the microRNA-181c/ TNF-α/tight junction axis

Shen, Simin; Zhao, Jingjiao; Dai, Yicong; Chen, Fengrong; Zhang, Zunyue; Yu, Juehua; Wang, Kunhua

doi:10.1016/j.toxlet.2019.12.020

Cited by 31 publications

(20 citation statements)

References 30 publications

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“…Previous studies of methamphetamine-treated intestinal tissues concentrated primarily on the mechanisms involved in amphetamine transport and efflux (25). A handful of recent studies reported that the administration of methamphetamine causes gut dysbiosis and activates proinflammatory factors in the epithelium (11)(12)(13). Alternatively, release of dopamine and other neurotransmitters induced by methamphetamine can also have multiple harmful effects on the gastrointestinal system.…”

Section: Discussionmentioning

confidence: 99%

“…Both the permeability of and endotoxins in the intestinal tissue of methamphetamine-treated mice were preceded by histological evidence of inflammation in the ileum colon junction. Another study reported that methamphetamine caused intestinal barrier lesions in a monolayer cell model and in methamphetamine-dependent people with inflammatory cytokine tumor necrosis factor-α release (13).…”

Section: Discussionmentioning

confidence: 99%

“…Another cellular study found that methamphetamine can cause NLRP3 inflammasome overexpression and severe intestinal inflammatory injury (12). Furthermore, inhibiting the expression of microRNA (miRNA) 181c, which directly targets and regulates tumor necrosis factor-α, has been shown to induce intestinal epithelial apoptosis, causing damage to the intestinal barrier (13). However, the mechanism of methamphetamine use impairs the immune function and the intestinal barrier remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Intestinal mRNA expression profile and bioinformatics analysis in a methamphetamine-induced mouse model of inflammatory bowel disease

Sun

Chen

et al. 2020

Ann Transl Med

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Background: Methamphetamine use has become a serious global public health problem and puts increasing burdens on healthcare services. Abdominal complications caused by methamphetamine use are uncommon and often go ignored by clinicians. The exact intestinal pathological alterations and transcriptomic responses associated with methamphetamine use are not well understood. This study sought to investigate the transcriptome in a methamphetamine-induced mouse model of inflammatory bowel disease (IBD) using next-generation RNA sequencing.Methods: Tissues from the ileum of methamphetamine-treated mice (n=5) and control mice (n=5) were dissected, processed and applied to RNA-sequencing. Bioinformatics and histopathological analysis were then performed. The expression profiles of intestinal tissue samples were analyzed and their expression profiles were integrated to obtain the differentially expressed genes and analyzed using bioinformatics. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the differentially expressed genes were performed using Metascape.Results: A total of 326 differentially expressed genes were identified; of these genes, 120 were upregulated and 206 were downregulated. The Gene Ontology analysis showed that the biological processes of the differentially expressed genes were focused primarily on the regulation of cellular catabolic processes, endocytosis, and autophagy. The main cellular components included the endoplasmic and endocytic vesicles, cytoskeleton, adherens junctions, focal adhesions, cell body, and lysosomes. Molecular functions included protein transferase, GTPase and proteinase activities, actin-binding, and protein-lipid complex binding.The Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the differentially expressed genes were mainly involved in bacterial invasion of epithelial cells, protein processing in the endoplasmic reticulum, regulation of the actin cytoskeleton, and T-cell receptor signaling pathways. A set of overlapping genes between IBD and methamphetamine-treated intestinal tissues was discovered. Conclusions:The present study is the first to analyze intestinal samples from methamphetamine-treated mice using high-throughput RNA sequencing. This study revealed key molecules that might be involved in

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Intestinal mRNA expression profile and bioinformatics analysis in a methamphetamine-induced mouse model of inflammatory bowel disease

Sun

Chen

et al. 2020

Ann Transl Med

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“…A recent study showed that ethanol binges mainly induced bacterial translocation to the mesenteric lymph nodes and activation of immune systems in rats [69]. Methamphetamine also induced the release of TNF‐α, which leads to intestinal barrier lesion in humans by inducing apoptosis in epithelial cells and altering the structure and function of tight junctions [70]. These studies reveal the possibility that the drug interacts with the intestine and induces a proinflammatory response in the systemic circulation and peripheral organs.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2020

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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.

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“…As a chronic and relapsing brain disease (1,2), heroin addiction is usually characterized by sensitization, dependence, and compulsive drug use (3,4). Beyond neuropsychiatric disorders, our previous studies showed that heroin abuse is often associated with decreased appetite, constipation, nutritional and gastrointestinal symptoms that can lead to low abstinence rate and malnutrition or nutritional risks during the withdrawal period (5)(6)(7). More seriously, drug-induced intestinal barrier lesions and severe enterogenic infections or related death were observed in Rhesus monkeys (5) and methamphetamine treated mice (8).…”

Section: Introductionmentioning

confidence: 99%

The Association of Altered Gut Microbiota and Intestinal Mucosal Barrier Integrity in Mice With Heroin Dependence

et al. 2021

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The gut microbiota is believed to play a significant role in psychological and gastrointestinal symptoms in heroin addicts. However, the underlying mechanism remains largely unknown. We show here that heroin addicts had a decrease in body mass index (BMI) and abnormal serum D-lactic acid (DLA), endotoxin (ET) and diamine oxidase (DAO) levels during their withdrawal stage, suggesting a potential intestinal injury. The gut microbial profiles in the mouse model with heroin dependence showed slightly decreased alpha diversity, as well as higher levels of Bifidobacterium and Sutterella and a decrease in Akkermansia at genus level compared to the control group. Fecal microbiota transplantation (FMT) further confirmed that the microbiota altered by heroin dependence was sufficient to impair body weight and intestinal mucosal barrier integrity in recipient mice. Moreover, short-chain fatty acids (SCFAs) profiling revealed that microbiota-derived propionic acid significantly decreased in heroin dependent mice compared to controls. Overall, our study shows that heroin dependence significantly altered gut microbiota and impaired intestinal mucosal barrier integrity in mice, highlighting the role of the gut microbiota in substance use disorders and the pathophysiology of withdrawal symptoms.

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Methamphetamine-induced alterations in intestinal mucosal barrier function occur via the microRNA-181c/ TNF-α/tight junction axis

Cited by 31 publications

References 30 publications

Intestinal mRNA expression profile and bioinformatics analysis in a methamphetamine-induced mouse model of inflammatory bowel disease

Intestinal mRNA expression profile and bioinformatics analysis in a methamphetamine-induced mouse model of inflammatory bowel disease

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

The Association of Altered Gut Microbiota and Intestinal Mucosal Barrier Integrity in Mice With Heroin Dependence

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