Abstract
Cytokines are one of the most important components of the immune system. They orchestrate the brain's response to infectious and other exogenous insults and are crucial mediators of the cross-talk between the nervous and immune systems. Epidemiological studies have demonstrated that severe infections and autoimmune disorders, in addition to genetic predisposition, are risk factors for schizophrenia. Furthermore, maternal infection during pregnancy appears to increase the risk of schizophrenia, and proinflammatory cytokines may be negatively involved in the neurodevelopmental process. A cytokine imbalance has been described in the blood and cerebrospinal fluid of schizophrenia patients, particularly in the T helper type 1 [Th1] and type 2 [Th2] cytokines, albeit the results of such studies appear to be contradictory. Chronic stress, likewise, appears to contribute to a lasting proinflammatory state and likely also promotes the disorder. The aim of this mini-review is to investigate the roles of different cytokines in the pathophysiology of schizophrenia and define how cytokines may represent key molecular targets to regulate for the prevention and treatment of schizophrenia. How current antipsychotic drugs impact cytokine networks is also evaluated. In this context, we propose to change the focus of schizophrenia from a traditionally defined brain disorder, to one that is substantially impacted by the periphery and immune system.
Highlights
Schizophrenia, a chronic and often debilitating mental disorder, impacts ∼1% of the world’s population and generally occurs in late adolescence or early adulthood
We first define what cytokines are and where they derive from. We review their involvement in schizophrenia, in relation to studies that have quantified elevations and declines of select cytokines in the periphery or central nervous system (CNS)
Results showed that patients with first-episode psychosis and those with acute relapse of psychosis had significantly elevated levels of IL-1β, IL6, tumor necrosis factor-α (TNF-α), IFN-γ, and IL-12, and patients under antipsychotic treatment showed a significant decline in IL-6, IL-1β, and IFN-γ and a rise in IL-12 and soluble IL-2 receptor
Summary
Schizophrenia, a chronic and often debilitating mental disorder, impacts ∼1% of the world’s population and generally occurs in late adolescence or early adulthood. An increasing number of studies indicating a role of inflammation and immunity in the pathogenesis of symptoms of schizophrenia have provided evidence that systemic inflammation can exert a profound influence on the brain that leads to changes in mood, cognition, and behavior. In this regard, the peripheral immune system-to-brain communication pathways have been studied extensively in the context of other neuroinflammmatory diseases in which inflammatory cytokines are, likewise, considered to play a critical role [15,16,17]. It is possible to speculate that abnormal levels of cytokines could potentially be used as a disease indicator and may provide a diagnostic or prognostic biomarker in schizophrenia [21, 22]
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