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].