Protective effects of interferon-γ against methamphetamine-induced neurotoxicity

Hozumi, Hiroaki; Asanuma, Masato; Miyazaki, Ikuko; Fukuoka, Saki; Kikkawa, Yuri; Kimoto, Naotaka; Kitamura, Yoshihisa; Sendo, Toshiaki; Kita, Taizo; Gomita, Yutaka

doi:10.1016/j.toxlet.2008.01.005

Cited by 24 publications

(14 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, IFN-γ (another proinflammatory cytokine) injected systemically prior to repeated methamphetamine exposure protects against methamphetamine-induced neurotoxicity (as measured by a reduction in striatal dopamine transporters) and hyperthermia, putatively through intracerebralmolecular pathways (Hozumi et al, 2008). Thus, of the altered immune factors, some cytokines appear to facilitate or promote methamphetamine-induced toxicities but others may slow or prevent the development of adverse drug effects.…”

Section: Partmentioning

confidence: 99%

Neuroimmune Basis of Methamphetamine Toxicity

Loftis

Janowsky

2014

International Review of Neurobiology

105

View full text Add to dashboard Cite

Although it is not known which antigen-specific immune responses (or if antigen-specific immune responses) are relevant or required for methamphetamine's neurotoxic effects, it is apparent that methamphetamine exposure is associated with significant effects on adaptive and innate immunity. Alterations in lymphocyte activity and number, changes in cytokine signaling, impairments in phagocytic functions, and glial activation and gliosis have all been reported. These drug-induced changes in immune response, particularly within the CNS, are now thought to play a critical role in the addiction process for methamphetamine dependence as well as for other substance use disorders. In Section 2, methamphetamine's effects on glial cell (e.g., microglia and astrocytes) activity and inflammatory signaling cascades are summarized, including how alterations in immune cell function can induce the neurotoxic and addictive effects of methamphetamine. Section 2 also describes neurotransmitter involvement in the modulation of methamphetamine's inflammatory effects. Section 3 discusses the very recent use of pharmacological and genetic animal models which have helped elucidate the behavioral effects of methamphetamine's neurotoxic effects and the role of the immune system. Section 4 is focused on the effects of methamphetamine on blood–brain barrier integrity and associated immune consequences. Clinical considerations such as the combined effects of methamphetamine and HIV and/or HCV on brain structure and function are included in Section 4. Finally, in Section 5, immune-based treatment strategies are reviewed, with a focus on vaccine development, neuroimmune therapies, and other anti-inflammatory approaches.

show abstract

Section: Partmentioning

confidence: 99%

Neuroimmune Basis of Methamphetamine Toxicity

Loftis

Janowsky

2014

International Review of Neurobiology

105

View full text Add to dashboard Cite

show abstract

“…However, reserpine inducing hypothermia does not prevent the neurotoxic effects of METH (14). In addition, IFN-γ completely prevents the neurotoxicity to dopaminergic neurons but does not alter METH-induced hyperthermia (15). These findings suggest that hyperthermia might contribute to, but is not the sole cause of, the neuropathology produced by METH or MDMA.…”

mentioning

confidence: 81%

Protective Effects of Isoliquiritigenin Against Methamphetamine-Induced Neurotoxicity in Mice

Lee¹,

Yang²,

Jeon³

et al. 2009

J Pharmacol Sci

View full text Add to dashboard Cite

Abstract. Isoliquiritigenin (ISL) suppresses cocaine-induced extracellular dopamine levels and has a neuroprotective effect in cocaine-treated rat brain. Here, we examine the effect of ISL on methamphetamine-induced striatal neurotoxicity. Repeated injections of methamphetamine cause the loss of striatal dopamine transporter (DAT) and tyrosine hydroxylase (TH). Intraperitoneal injection of ISL prior to methamphetamine injection significantly prevented methamphetamineinduced reduction of DAT and TH. ISL also suppressed methamphetamine-induced activation of glial cells. Moreover, ISL impeded the expression of nitric oxide synthase and the activation of NF-κB through blockage of its phosphorylation. Our results suggest that ISL protects against methamphetamine-induced neurotoxicity by inhibition of NF-κB activation.

show abstract

“…Recent studies have shown that METH abuse is associated with an increased risk of human immunodeficiency virus (HIV) infection, hepatitis B and C infections, and other diseases (Halkitis et al, 2001;Gonzales et al, 2006;Miller et al, 2009). Emerging studies have demonstrated that METH can alter the production of both inflammatory and anti-inflammatory cytokines in the periphery (Yu et al, 2002a,b;Hozumi et al, 2008). METH also causes immune dysfunction in mature mammals by negatively altering antibody and cytokine production in mice .…”

Section: Introductionmentioning

confidence: 99%

The dopamine D3 receptor regulates the effects of methamphetamine on LPS-induced cytokine production in murine mast cells

Ren

et al. 2015

Immunobiology

View full text Add to dashboard Cite

Protective effects of interferon-γ against methamphetamine-induced neurotoxicity

Cited by 24 publications

References 34 publications

Neuroimmune Basis of Methamphetamine Toxicity

Neuroimmune Basis of Methamphetamine Toxicity

Protective Effects of Isoliquiritigenin Against Methamphetamine-Induced Neurotoxicity in Mice

The dopamine D3 receptor regulates the effects of methamphetamine on LPS-induced cytokine production in murine mast cells

Contact Info

Product

Resources

About