Abstract
Drug abuse is a universal phenomenon that happens across the world. And the neurotoxicity caused by drug abuse in the central nervous system has been extensively studied during the last decade. More recently, the role of drugs causing neuroinflammation, which would subsequently affect dopaminergic neurotoxicity, has aroused wide attention. This paper aims to present a literature review of the studies on the role of the interleukin family in substance-dependent neuroinflammation. Currently, the most studied cytokines in the interleukin family in the drug field are IL-1 and IL-6. In addition, based on the previous literature on changes in interleukin in neuroinflammation induced by different drugs, this paper identifies neuroinflammation-related diseases caused by interleukin families, and summarizes recent advances in the dynamics, mechanisms, immunomodulatory and anti-inflammatory effects that are related to the pathogenesis of these diseases. In conclusion, this review elucidates substance-dependent neurotoxicity from the perspective of interleukin alterations.
1. Introduction
Drug addiction is a worldwide problem characterized by physical and psychological dependence on drugs, which results in increasing urges to seek and take drugs, loss of control over drug intake, and withdrawal symptoms[1]. Globally, approximately 40 million people with substance use disorders (SUD) currently require addiction treatment services, and there are roughly 600,000 drug-related deaths annually[2]. The most commonly used drugs over the world include heroin, methamphetamine and cocaine. And the use of these drugs would depress some central nervous system (CNS) functions[3].
For many years, the CNS was thought to be immune-specific due to its lack of a typical immunological response to foreign antigens. However, it is now generally accepted that neuroinflammation is characterized by the infiltration of circulating immune cells, including neutrophils and monocytes, while other resident cells such as microglia (key immune cells of the central nervous system) and astrocytes Glial cells also infiltrate[4]. Among all these mediators in CNS, the interleukin (IL) family of proinflammatory cytokines is the most widely studied. Therefore, in terms of drug-induced neuroinflammation and treatment, it is of great significance to understand the role of the IL family in the CNS, the mechanism of IL action and the regulation of IL-1 activity[4, 5]. Although the mechanism of action of IL in neuronal damage caused by different drugs remains unclear, several possible pathways have been identified, which will be discussed as follows[4].