Dual roles of interleukin-33 in cognitive function by regulating central nervous system inflammation

Abstract

With the advent of an aging society, the incidence of dementia is increasing, resulting in a vast burden on society. It is increasingly acknowledged that neuroinflammation is implicated in various neurological diseases with cognitive dysfunction such as Alzheimer’s disease, multiple sclerosis, ischemic stroke, traumatic brain injury, and central nervous system infections. As an important neuroinflammatory factor, interleukin-33 (IL-33) is highly expressed in various tissues and cells in the mammalian brain, where it plays a role in the pathogenesis of a number of central nervous system conditions. Reams of previous studies have shown that IL-33 has both pro- and anti-inflammatory effects, playing dual roles in the progression of diseases linked to cognitive impairment by regulating the activation and polarization of immune cells, apoptosis, and synaptic plasticity. This article will summarize the current findings on the effects IL-33 exerts on cognitive function by regulating neuroinflammation, and attempt to explore possible therapeutic strategies for cognitive disorders based on the adverse and protective mechanisms of IL-33.

Berberine promotes immunological outcomes and decreases neuroinflammation in the experimental model of multiple sclerosis through the expansion of Treg and Th2 cells

“…IL‐27 typically produced by antigen‐presenting cells (APCs) can decrease EAE severity through a variety of processes, such as diminishing Th17 cell differentiation and enhancing the production of IL‐10 12,13 . In other anti‐inflammatory cytokines, IL‐33 treatment may have a positive effect on the EAE treatment process by switching from predominantly Th1/Th17 pathogenic cells to Th2 and Treg cells 14 . IL‐35 is another suppressor cytokine mainly released by Treg cells that are required for the maximum inhibitory effect of mouse Treg cells in vitro and in vivo 15 …”

“…12,13 In other anti-inflammatory cytokines, IL-33 treatment may have a positive effect on the EAE treatment process by switching from predominantly Th1/ Th17 pathogenic cells to Th2 and Treg cells. 14 IL-35 is another suppressor cytokine mainly released by Treg cells that are required for the maximum inhibitory effect of mouse Treg cells in vitro and in vivo. 15 To date, a variety of anti-inflammatory and immunoregulatory therapies are used to prevent the progress of MS, but they are only several partially effective treatments to modify the disease course.…”

“… 12 , 13 In other anti‐inflammatory cytokines, IL‐33 treatment may have a positive effect on the EAE treatment process by switching from predominantly Th1/Th17 pathogenic cells to Th2 and Treg cells. 14 IL‐35 is another suppressor cytokine mainly released by Treg cells that are required for the maximum inhibitory effect of mouse Treg cells in vitro and in vivo. 15 …”

IL-33 Alleviates Postoperative Cognitive Impairment by Inhibiting Hippocampal Inflammation and Upregulating Excitatory Synaptic Number in Aged Mice

“…IL-33 plays a key role in learning and memory via regulating hippocampal inflammation and synaptic plasticity [ 24 ], but the underlying molecular and cellular mechanisms in dNCR remain unclear. Our study showed that surgery/anesthesia induced postoperative cognitive impairment accompanied by decreased astrocyte-derived IL-33 in aged mice.…”

“…IL-33 has been shown to affect cognitive function by modulating neuroinflammation, synaptic plasticity, apoptosis and autophagy [ 24 ]. Numerous studies have shown that the overactivation of microglia and the release of inflammatory factors (e.g., TNF-α, IL-1β, IL-6 and IL-10) induce the occurrence of dNCR by impairing neuronal function [ 20 , 32 ].…”