NLRP3 inflammasome activation underlies the neuro-oxidative stress associated with Methamphetamine (METH) and SARS-CoV2 induced co-morbidity in human microglia-Reference-Cited by-同舟云学术

NLRP3 inflammasome activation underlies the neuro-oxidative stress associated with Methamphetamine (METH) and SARS-CoV2 induced co-morbidity in human microglia

Published:2023-06-26 Issue:3 Volume:2 Page:245-252
ISSN:2750-6665
Container-title:NeuroImmune Pharmacology and Therapeutics
language:en
Short-container-title:

Author:

Machhar Janvhi Suresh¹,Abou-Jaoude Elias¹,Schwartz Stanley A.¹,Aalinkeel Ravikumar¹,Mahajan Supriya D.¹

Affiliation:

1. Department of Medicine, Division of Allergy, Immunology, and Rheumatology, Jacobs School of Medicine & Biomedical Sciences , University at Buffalo , Buffalo , NY , USA

Abstract

Abstract Acute and chronic use of Methamphetamine (METH) has critical immunological implications and METH users are more vulnerable to SARS-CoV2 infection. Inflammasomes are activated in response to SARS-CoV2 infection. METH also activates NLRP3 inflammasome in microglia and promotes neuro cognitive deficits. The goal of the study was to examine the involvement of NLRP3 inflammasome in METH and/or SARS-CoV2 induced neuro-oxidative stress in microglial cells. Our results suggests that METH +/− SARS-CoV2 initiated a neuro immune-inflammatory response and mitochondrial oxidative stress via NLRP3 inflammasome activation induced increased Caspase −1 and increased lipid peroxidation. Our data suggests that SARS-CoV2 infection in METH abusing subjects may result in long-term neurological deficits resulting from microglial dysfunction and apoptosis attributed to NLRP3 inflammasome activation.

Funder

National Institute of Drug Abuse

Publisher

Walter de Gruyter GmbH

Link

https://www.degruyter.com/document/doi/10.1515/nipt-2023-0005/pdf

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