Inflammasome in drug abuse

Enquan Xu, Jianuo Liu, Xiaobei Wang, Huangui Xiong

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Drug abuse disorders refer to a set of related negative health implications associated with compulsive drug seeking and use. Because almost all addictive drugs act on the brain, many of them cause neurological impairments after long-term abuse. Neuropathological studies have revealed a widespread impairment of the cellular elements. As the key components to limit the damage of neural cells, CNS immune system is also found affected by these drugs, directly or indirectly. It has been shown that drugs of abuse alter neuroimmune gene expression and signaling. Growing studies on neuroimmune factors further demonstrate their indispensable role in drugs-induced neurotoxicity. As an important proinflammatory intracellular receptor, inflammasome is activated in many neurodegenerative diseases in response to a broad range of damage-associated molecular patterns (DAMPs) signals. In the cases of drug abuse, especially in those with comorbid of HIV infection and sustained pain, inflammasome activation significantly promotes the neuroinflammation-associated toxicities. To understand inflammasome in drug-associated neurotoxic activity, we reviewed the role played by inflammasome in drug abuse-induced microglial neurotoxicity and evaluated the potential of imflammasone as a therapeutic target for drug abuse disorders based on recent development of various selective small-molecular inflammasome inhibitors.

Original languageEnglish (US)
Article numberIJPPP0069071
Pages (from-to)165-177
Number of pages13
JournalInternational Journal of Physiology, Pathophysiology and Pharmacology
Volume9
Issue number6
StatePublished - Jan 1 2017

Fingerprint

Inflammasomes
Substance-Related Disorders
Pharmaceutical Preparations
Street Drugs
Neurodegenerative Diseases
HIV Infections
Immune System
Gene Expression
Pain
Health
Brain

Keywords

  • Drug abuse
  • Microglia
  • NLRP3
  • Neuroinflammation
  • Proinflammatory cytokines

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Physiology
  • Physiology (medical)

Cite this

Inflammasome in drug abuse. / Xu, Enquan; Liu, Jianuo; Wang, Xiaobei; Xiong, Huangui.

In: International Journal of Physiology, Pathophysiology and Pharmacology, Vol. 9, No. 6, IJPPP0069071, 01.01.2017, p. 165-177.

Research output: Contribution to journalArticle

Xu, E, Liu, J, Wang, X & Xiong, H 2017, 'Inflammasome in drug abuse', International Journal of Physiology, Pathophysiology and Pharmacology, vol. 9, no. 6, IJPPP0069071, pp. 165-177.
Xu, Enquan ; Liu, Jianuo ; Wang, Xiaobei ; Xiong, Huangui. / Inflammasome in drug abuse. In: International Journal of Physiology, Pathophysiology and Pharmacology. 2017 ; Vol. 9, No. 6. pp. 165-177.
@article{4faffb0de01f4cb48849729c096386cb,
title = "Inflammasome in drug abuse",
abstract = "Drug abuse disorders refer to a set of related negative health implications associated with compulsive drug seeking and use. Because almost all addictive drugs act on the brain, many of them cause neurological impairments after long-term abuse. Neuropathological studies have revealed a widespread impairment of the cellular elements. As the key components to limit the damage of neural cells, CNS immune system is also found affected by these drugs, directly or indirectly. It has been shown that drugs of abuse alter neuroimmune gene expression and signaling. Growing studies on neuroimmune factors further demonstrate their indispensable role in drugs-induced neurotoxicity. As an important proinflammatory intracellular receptor, inflammasome is activated in many neurodegenerative diseases in response to a broad range of damage-associated molecular patterns (DAMPs) signals. In the cases of drug abuse, especially in those with comorbid of HIV infection and sustained pain, inflammasome activation significantly promotes the neuroinflammation-associated toxicities. To understand inflammasome in drug-associated neurotoxic activity, we reviewed the role played by inflammasome in drug abuse-induced microglial neurotoxicity and evaluated the potential of imflammasone as a therapeutic target for drug abuse disorders based on recent development of various selective small-molecular inflammasome inhibitors.",
keywords = "Drug abuse, Microglia, NLRP3, Neuroinflammation, Proinflammatory cytokines",
author = "Enquan Xu and Jianuo Liu and Xiaobei Wang and Huangui Xiong",
year = "2017",
month = "1",
day = "1",
language = "English (US)",
volume = "9",
pages = "165--177",
journal = "International Journal of Physiology, Pathophysiology and Pharmacology",
issn = "1944-8171",
publisher = "e-Century Publishing Corporation",
number = "6",

}

TY - JOUR

T1 - Inflammasome in drug abuse

AU - Xu, Enquan

AU - Liu, Jianuo

AU - Wang, Xiaobei

AU - Xiong, Huangui

PY - 2017/1/1

Y1 - 2017/1/1

N2 - Drug abuse disorders refer to a set of related negative health implications associated with compulsive drug seeking and use. Because almost all addictive drugs act on the brain, many of them cause neurological impairments after long-term abuse. Neuropathological studies have revealed a widespread impairment of the cellular elements. As the key components to limit the damage of neural cells, CNS immune system is also found affected by these drugs, directly or indirectly. It has been shown that drugs of abuse alter neuroimmune gene expression and signaling. Growing studies on neuroimmune factors further demonstrate their indispensable role in drugs-induced neurotoxicity. As an important proinflammatory intracellular receptor, inflammasome is activated in many neurodegenerative diseases in response to a broad range of damage-associated molecular patterns (DAMPs) signals. In the cases of drug abuse, especially in those with comorbid of HIV infection and sustained pain, inflammasome activation significantly promotes the neuroinflammation-associated toxicities. To understand inflammasome in drug-associated neurotoxic activity, we reviewed the role played by inflammasome in drug abuse-induced microglial neurotoxicity and evaluated the potential of imflammasone as a therapeutic target for drug abuse disorders based on recent development of various selective small-molecular inflammasome inhibitors.

AB - Drug abuse disorders refer to a set of related negative health implications associated with compulsive drug seeking and use. Because almost all addictive drugs act on the brain, many of them cause neurological impairments after long-term abuse. Neuropathological studies have revealed a widespread impairment of the cellular elements. As the key components to limit the damage of neural cells, CNS immune system is also found affected by these drugs, directly or indirectly. It has been shown that drugs of abuse alter neuroimmune gene expression and signaling. Growing studies on neuroimmune factors further demonstrate their indispensable role in drugs-induced neurotoxicity. As an important proinflammatory intracellular receptor, inflammasome is activated in many neurodegenerative diseases in response to a broad range of damage-associated molecular patterns (DAMPs) signals. In the cases of drug abuse, especially in those with comorbid of HIV infection and sustained pain, inflammasome activation significantly promotes the neuroinflammation-associated toxicities. To understand inflammasome in drug-associated neurotoxic activity, we reviewed the role played by inflammasome in drug abuse-induced microglial neurotoxicity and evaluated the potential of imflammasone as a therapeutic target for drug abuse disorders based on recent development of various selective small-molecular inflammasome inhibitors.

KW - Drug abuse

KW - Microglia

KW - NLRP3

KW - Neuroinflammation

KW - Proinflammatory cytokines

UR - http://www.scopus.com/inward/record.url?scp=85054478058&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85054478058&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:85054478058

VL - 9

SP - 165

EP - 177

JO - International Journal of Physiology, Pathophysiology and Pharmacology

JF - International Journal of Physiology, Pathophysiology and Pharmacology

SN - 1944-8171

IS - 6

M1 - IJPPP0069071

ER -