Abstract
Background: A growing body of evidence shows that immune system disorders are one of the important etiological factors of schizophrenia. Inflammatory cytokines play a very critical role in the pathogenesis and treatment of schizophrenia. However, in the actual clinical practice, there is still a lack of confirmed biological indicators that can be used to evaluate the therapeutic effect of antipsychotics.Methods: In this study, 82 male patients with first-episode schizophrenia and 30 healthy controls were included. The Positive and Negative Syndrome Scale (PANSS) scores were evaluated, and the serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin 1β (IL-1β), interleukin 6 (IL-6), interleukin 17 (IL-17), and transforming growth factor β1 (TGF-β1) were detected, both at baseline and 4 weeks later. The patients were divided into two groups, the effective group and the ineffective group, according to the reduction rate of PANSS.Results: In the case group, the levels of hs-CRP were significantly elevated (p = 0.00), whereas IL-1β, IL-6, and IL-17 were significantly reduced as compared to the baseline (p = 0.01, 0.02, and 0.00, respectively). Importantly, the baseline levels of the five inflammatory factors were significantly higher in the case group as compared to the control group (p = 0.00, 0.00, 0.00, 0.00, and 0.00, respectively). Post-treatment, the serum levels for IL-1β, IL-6, and IL-17 were significantly higher in the effective group than in the ineffective group (p = 0.00, 0.00, and 0.01, respectively). For every increase in the amount of IL-1β, the risk of ineffectiveness increased by 7% (OR = 0.93 [0.86–1.00]; p = 0.04), whereas for every increase in the amount of IL-17, the risk of ineffectiveness increased by 5% (OR = 0.95 [0.90–0.99]; p = 0.03).Conclusion: The results of the study showed that the levels of inflammatory factors in patients with different therapeutic effects were different, and the changes in the amounts of IL-1β and IL-17 acted as predictors of poor efficacy.
Highlights
In the past few decades, significant evidence established the idea that the complex interaction between the immune-inflammatory system and the brain might have important etiological and therapeutic significance with regard to neuropsychiatric diseases [1]
The following were the inclusion criteria for subject selection: [1] patients meeting the diagnostic criteria of schizophrenia as per the International Classification of Diseases 10th Revision (ICD-10), with a disease course of ≤60 months and no antipsychotic treatment or treatment time of
For every increase in the amount of IL-1β, the risk of ineffectiveness increased by 7% (OR = 0.93 [0.86–1.00]; p = 0.04); and for every increase in the amount of IL-17, the risk of ineffectiveness increased by 5% (OR = 0.95 [0.90–0.99]; p = 0.03) (Table 5)
Summary
In the past few decades, significant evidence established the idea that the complex interaction between the immune-inflammatory system and the brain might have important etiological and therapeutic significance with regard to neuropsychiatric diseases [1]. An animal study showed that atypical antipsychotics such as clozapine and olanzapine have the unique effect of inhibiting the levels of proinflammatory factors [9]. Another example, in vitro assessment of second-generation antipsychotic drugs, reported a reduction in the mRNA expression levels for IL-1β, IL-6, and TNF-α in the peripheral blood of healthy people, which further resulted in a reduction in the concentration of these inflammatory factors [10]. The occurrence of inflammatory state during psychosis and the accumulated evidence for anti-inflammatory effects of antipsychotic drugs support the use of inflammation as a potential new therapeutic target for the management of schizophrenia. In the actual clinical practice, there is still a lack of confirmed biological indicators that can be used to evaluate the therapeutic effect of antipsychotics
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