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The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

ABSTRACT: The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

PROVIDER: PRJNA892117 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21973641.fastq.gz	Fastqsanger.gz
	SRR21973642.fastq.gz	Fastqsanger.gz
	SRR21973643.fastq.gz	Fastqsanger.gz
	SRR21973644.fastq.gz	Fastqsanger.gz
	SRR21973645.fastq.gz	Fastqsanger.gz

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The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

Project description:Fentanyl enhanced expression of CXCR4 and CCR5 protein levels and viral expression in a dose-dependent manner in multiple HIV-susceptible and HIV-infected cell lines. Multiple genes associated with apoptosis, antiviral / interferon response, chemokine. signaling, and NFκB signaling were differentially regulated by fentanyl. Thus fentanyl impacts HIV replication and chemokine co-receptor expression in HIV-susceptible and HIV-infected lymphocyte cell lines suggesting that opioid use may increase the likelihood of transmission to others and accelerate disease progression.

2022-10-20 | GSE216124 | GEO

The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

Project description:The illicit use of synthetic opioids such as fentanyl has led to a serious public health crisis in the United States. People with opioid use disorder are more likely to contract infections such as HIV and viral hepatitis. While several drugs of abuse are known to enhance viral replication and to suppress immunologic responses, the effects of synthetic opioids on HIV pathogenesis have not been investigated thoroughly. Thus, we examined the impact of fentanyl on HIV-susceptible and HIV-infected cell types and chemokine receptor expression in vitro. TZM-bl and HIV-infected lymphocyte cells were incubated with fentanyl at concentrations of 1 ng, 100 ng, and 10 ug. Expression levels of the CXCR4 and CCR5 chemokine receptors were measured in cell lysates, and HIV p24 antigen was quantified in culture supernatants by ELISA. HIV proviral DNA was quantified in cells using SYBR RT-PCR targeting the pol gene. Cell viability in the presence of drug was detected by the MTT Cell Proliferation Assay. RNA-seq and miRNAseq was performed to characterize cellular gene regulation in the presence of fentanyl. Fentanyl enhanced expression of CXCR4 and CCR5 protein levels in a dose-dependent manner in HIV-susceptible and HIV-infected cells. Similarly, fentanyl induced viral expression in HIV-exposed TZM-bl cells and in multiple HIV-infected lymphocyte cell lines. Multiple genes associated with apoptosis, antiviral / interferon response, chemokine signaling, and NFκB signaling were differentially regulated by fentanyl. These data demonstrate that the synthetic opioid fentanyl impacts HIV replication and chemokine co-receptor expression in HIV-susceptible and HIV-infected cells. Increased virus levels also suggest that opioid use may increase the likelihood of transmission to others and accelerate disease progression.

2022-10-19 | GSE216044 | GEO

The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

Project description:The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

| PRJNA891755 | ENA

The synthetic opioid fentanyl increases HIV replication expression in macrophages

Project description:The illicit use of synthetic opioids such as fentanyl has led to a serious public health crisis in the US. People with opioid use disorder are more likely to contract infections such as HIV and viral hepatitis and experience more severe disease. While several drugs of abuse are known to enhance viral replication and to suppress immunologic responses, the effects of synthetic opioids on HIV pathogenesis have not been investigated thoroughly. Thus, we examined the impact of fentanyl on macrophage cell line U937 and monocyte derived macrophage cells and chemokine receptor expression in vitro.

2024-08-28 | GSE241769 | GEO

Opioid withdrawal produces sex-specific effects on fentanyl-vs.-food choice and mesolimbic transcription

Project description:Background: Opioid withdrawal is a key driver of opioid addiction and an obstacle to recovery. However, withdrawal effects on opioid reinforcement and mesolimbic neuroadaptation are understudied and the role of sex is largely unknown. Methods: Male (n=13) and female (n=12) rats responded under a fentanyl-vs.-food “choice” procedure during daily 2h sessions. In addition to the daily choice sessions, rats were provided extended access to fentanyl during 12h self-administration sessions. After two weeks of this selfadministration regimen, the nucleus accumbens (NAc) and ventral tegmental area (VTA) of a subset of rats were subjected to RNA sequencing. In the remaining rats, a third week of this self-administration regimen was conducted, during which methadone effects on fentanyl-vs.-food choice were determined. Results: Prior to opioid dependence, male and female rats similarly allocated responding between fentanyl and food. Abstinence from extended fentanyl access elicited similar increases in somatic withdrawal signs in both sexes. Despite similar withdrawal signs and extended access fentanyl intake, opioid withdrawal was accompanied by a maladaptive increase in fentanyl choice in males, but not females. Behavioral sex differences corresponded with a greater number of differentially expressed genes in the NAc and VTA of opioidwithdrawn females relative to males. Methadone blocked withdrawal-associated increases in fentanyl choice in males, but failed to further decrease fentanyl choice in females. Conclusions: These results provide foundational evidence of sex-specific neuroadaptations to opioid withdrawal, which may be relevant to the female-specific resilience to withdrawal-associated increases in opioid choice and aid in the identification of novel therapeutic targets.

2021-05-06 | GSE173959 | GEO

The synthetic opioid fentanyl increases HIV replication expression in macrophages

Project description:The synthetic opioid fentanyl increases HIV replication expression in macrophages

| PRJNA1009840 | ENA

Changes in gut microbiome composition drive fentanyl intake and striatal proteomic changes

Project description:Opioid use disorder (OUD) is a public health crisis currently being exacerbated by increases in use of fentanyl; therefore, the identification of novel biomarkers and treatment strategies is critical. Here, we define how manipulations of the gut microbiome drive fentanyl intake, fentanyl seeking, and alter proteomic plasticity in the nucleus accumbens. These findings establish clear relevance for gut-brain signaling in OUD, and lay foundations for further translational work in this space.

2024-05-22 | PXD035810 | Pride

Investigating the Risk of Arrhythmogenesis Associated with Fentanyl Abuse Using Mice and Human iPSC-Derived Cardiomyocytes

Project description:The rise in synthetic opioid use, particularly fentanyl, has severely exacerbated the opioid epidemic and its impact surged dramatically during the COVID-19 pandemic. Fentanyl, a prescription opioid used for anesthesia and analgesia, is 50-100x stronger than morphine. Opioid-induced cardiac arrest represents the most dramatic manifestation of the opioid use disorder. Fentanyl primarily targets opioid receptors (ORs) in the nervous system, but its misuse also adversely depresses the pulmonary and cardiovascular systems. The proarrhythmic effects of other opioids were reported; however, the electrophysiological consequences of fentanyl abuse have not been studied. Our analysis of 19 toxicology studies conducted between 1994 and 2022 found that the average blood concentration of fentanyl in abuse or overdose cases is 30±1 ng/mL (89 nM), ~3-fold higher than in chronic pain or ~7.5-fold higher than in occasionally exposed patients. Advances in human induced pluripotent stem cell (iPSC) technology provide unprecedented opportunities to study patient‐specific responses to opioid abuse. Human iPSC-derived cardiomyocytes (iPSC-CMs) from 3 healthy donors were exposed to three doses of 89 nM fentanyl for 5 days. Then, we investigated whether fentanyl abuse has any consequences on cardiac electrophysiology.

2025-09-03 | GSE287796 | GEO

The synthetic opioid fentanyl elicited transcriptomic alterations related to viral replication, immune response, and inflammation in vitro.

Project description:The US is in the midst of a major drug epidemic fueled in large part by the widespread recreational use of syntheticopioids such as fentanyl. we evaluated the impact of fentanyl using in cell lines that replicate infectious viruses. RNAseq identified a number of hepatocyte genes that were differentially regulated by fentanyl, including those related to apoptosis, the antiviral / interferon response, chemokine signaling, and NFkB signaling.

2021-04-21 | GSE167922 | GEO

Chronic opioid treatment arrests neurodevelopment and alters synaptic activity in human midbrain organoids

Project description:Understanding the impact of long-term opioid exposure on the embryonic brain is critical due to the surging number of pregnant mothers with opioid dependency, but has been limited by human brain inaccessibility and cross-species differences in animal models. Here we establish a human midbrain model that uses hiPSC-derived midbrain organoids and apply it to assess cell-type-specific responses to acute and chronic fentanyl treatment and fentanyl withdrawal. Single-cell mRNA sequencing of 25,510 cells from organoids in different treatment groups indicated that chronic fentanyl treatment arrests neuronal subtype specification during early midbrain development and alters synaptic activity and neuron projection. In contrast, acute fentanyl treatment increases dopamine release but does not significantly alter gene expression related to cell lineage development. These results provide the first examination of the effects of opioid exposure on human midbrain development at the single cell level.

2024-03-05 | GSE260711 | GEO

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