Inflammasome Activation by Methamphetamine Potentiates Lipopolysaccharide Stimulation of IL-1β Production in Microglia

Journal of Neuroimmune Pharmacology : the Official Journal of the Society on NeuroImmune Pharmacology
Enquan XuHuangui Xiong

Abstract

Methamphetamine (Meth) is an addictive psychostimulant abused worldwide. Ample evidence indicate that chronic abuse of Meth induces neurotoxicity via microglia-associated neuroinflammation and the activated microglia present in both Meth-administered animals and human abusers. The development of anti-neuroinflammation as a therapeutic strategy against Meth dependence promotes research to identify inflammatory pathways that are specifically tied to Meth-induced neurotoxicity. Currently, the exact mechanisms for Meth-induced microglia activation are largely unknown. NLRP3 is a well-studied cytosolic pattern recognition receptor (PRR), which promotes the assembly of the inflammasome in response to the danger-associated molecular patterns (DAMPs). It is our hypothesis that Meth activates NLRP3 inflammasome in microglia and promotes the processing and release of interleukin (IL)-1β, resulting in neurotoxic activity. To test this hypothesis, we studied the effects of Meth on IL-1β maturation and release from rat cortical microglial cultures. Incubation of microglia with physiologically relevant concentrations of Meth after lipopolysaccharide (LPS) priming produced an enhancement on IL-1β maturation and release. Meth treatment potenti...Continue Reading

References

Sep 1, 1994·Journal of Cellular Biochemistry·P A HillM C Meikle
Nov 26, 1998·The Journal of Biological Chemistry·M Garcia-CalvoN A Thornberry
Jan 31, 2004·Journal of the International Neuropsychological Society : JINS·Julie D RippethUNKNOWN HNRC Group
Feb 11, 2004·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Subramaniam JayanthiJean Lud Cadet
Mar 6, 2004·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Akira NakajimaToshitaka Nabeshima
Apr 15, 2004·Experimental Neurology·Matthew J LaVoieTeresa G Hastings
May 28, 2004·The Journal of Pharmacology and Experimental Therapeutics·David M ThomasDonald M Kuhn
Feb 3, 2005·Journal of Neurochemistry·David M Thomas, Donald M Kuhn
Jun 27, 2006·The AAPS Journal·Maria S Quinton, Bryan K Yamamoto
Jul 15, 2006·Progress in Neuro-psychopharmacology & Biological Psychiatry·Lin ZhangKenji Hashimoto
Sep 16, 2006·Molecular Aspects of Medicine·Eeva-Liisa Eskelinen
Apr 3, 2007·The Journal of Pharmacology and Experimental Therapeutics·M C ZerrateC A Pardo
Aug 19, 2007·Neuropsychology Review·J Cobb ScottIgor Grant
May 30, 2008·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Yoshimoto SekineJean L Cadet
Jul 8, 2008·Nature Immunology·Annett HalleDouglas T Golenbock
Oct 29, 2008·Oncogene·P Boya, G Kroemer
Mar 31, 2009·Brain Research Reviews·Irina N Krasnova, Jean Lud Cadet
Jul 29, 2009·Infection and Immunity·Zachary L NewmanMahtab Moayeri
Aug 6, 2009·Journal of Neuroimmune Pharmacology : the Official Journal of the Society on NeuroImmune Pharmacology·Carol A Colton
Aug 18, 2009·Apoptosis : an International Journal on Programmed Cell Death·Huan Ling LiangVani Nilakantan
Oct 6, 2009·Pharmacogenetics and Genomics·Liang LiuJanet K Coller
Feb 2, 2010·The International Journal on Drug Policy·Louisa DegenhardtUNKNOWN Reference Group to the United Nations on HIV and injecting drug use
Feb 20, 2010·Nature Reviews. Immunology·Jurg Tschopp, Kate Schroder
Mar 18, 2010·Nature Reviews. Neurology·V Hugh PerryClive Holmes
Jul 30, 2010·The Journal of Immunology : Official Journal of the American Association of Immunologists·Raghava PotulaYuri Persidsky
Aug 19, 2010·The American Journal on Addictions·Suzette Glasner-EdwardsUNKNOWN Methamphetamine Treatment Project Corporate Authors
Oct 1, 2010·Neurotherapeutics : the Journal of the American Society for Experimental NeuroTherapeutics·Melinda E Lull, Michelle L Block
Oct 5, 2010·Neuroscience and Biobehavioral Reviews·Karen Wager-Smith, Athina Markou
Dec 3, 2010·Nature·Rongbin ZhouJürg Tschopp
Jun 1, 2011·NeuroImage·Takeshi ShibaKen-ichi Yamada
Oct 25, 2011·Cytokine & Growth Factor Reviews·Gloria Lopez-Castejon, David Brough
Apr 24, 2012·Trends in Immunology·Richa HanamsagarTammy Kielian
Apr 26, 2012·Journal of Neuroinflammation·Fushan ShiDeming Zhao

❮ Previous
Next ❯

Citations

Apr 9, 2020·JAMA Psychiatry·Martin P Paulus, Jennifer L Stewart
Sep 10, 2019·Frontiers in Cellular Neuroscience·Xuebing ChenXia Yue
Feb 23, 2021·Journal of Neuroinflammation·Cassandra D GipsonErin E Maher
Mar 23, 2021·Journal of Neuroimmune Pharmacology : the Official Journal of the Society on NeuroImmune Pharmacology·Koffi L LakpaJonathan D Geiger
Jul 22, 2021·Archives of Pharmacal Research·Eun-Joo ShinHyoung-Chun Kim
Aug 26, 2021·Human Psychopharmacology·Yayan LuoNi Fan

❮ Previous
Next ❯

Methods Mentioned

BETA
PCR
ELISA
deubiquitination

Clinical Trials Mentioned

NCT01860807

Software Mentioned

OriginPro
Image J

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

Addiction

This feed focuses mechanisms underlying addiction and addictive behaviour including heroin and opium dependence, alcohol intoxication, gambling, and tobacco addiction.

Apoptotic Caspases

Apoptotic caspases belong to the protease enzyme family and are known to play an essential role in inflammation and programmed cell death. Here is the latest research.

Caspases in Metabolic Diseases

Caspases, the family of cysteine proteases are involved in programmed cell death, but their role in metabolic diseases, inflammation and immunity has been of interested. Discover the latest research on caspases in metabolic diseases here.

Antiphospholipid Syndrome

Antiphospholipid syndrome or antiphospholipid antibody syndrome (APS or APLS), is an autoimmune, hypercoagulable state caused by the presence of antibodies directed against phospholipids.