Abstract
Previous research has demonstrated aberrations in the levels of inflammatory cytokines in patients with schizophrenia (SCZ), but most of the respective studies have tested a narrow set of inflammatory cytokines. Here, we aimed to analyze broad immune profiles in the peripheral blood of the first-episode drug-free (FEDF) patients with SCZ at baseline and after an 8-week treatment with atypical antipsychotics. Serum samples from 24 FEDF patients with SCZ and 25 healthy control (HC) subjects were tested using Luminex multiplex analysis for 30 cytokines, chemokines, and growth factors. Multiple comparison tests demonstrated that interleukin-2 (IL-2), IL-4, interferon-gamma (IFN-γ), monokine induced by IFN-γ, and granulocyte colony-stimulating factor (G-CSF) levels were significantly increased, whereas those of the epidermal growth factor were significantly decreased in the FEDF patients with SCZ. Moreover, the levels of the 6 dysregulated cytokines as well as those of 12 additional soluble factors in FEDF patients with SCZ were significantly decreased after 8 weeks of antipsychotic treatment. Furthermore, the transcription of G-CSF and IFN-γ was significantly increased in FEDF patients with SCZ when compared with controls, and G-CSF and IFN-γ mRNA levels were highly correlated with their respective protein concentrations. Receiver operating characteristic curves showed that G-CSF and IFN-γ had good performance in differentiating between FEDF patients with SCZ and HC subjects. Taken together, our data revealed that FEDF patients with SCZ were accompanied by a unique pattern of immune profile, and antipsychotic medications seemed to suppress the immune function in these patients, which could be used to develop novel targets for the diagnosis and treatment of SCZ.
Highlights
Schizophrenia (SCZ) is a severe mental disorder that has profound effects on society and affects individuals and families [1, 2]
first-episode drug-free (FEDF), first-episode, drug-free; HC, healthy control; G-CSF, granulocyte colony-stimulating factors; IFN-γ, interferon gamma; MIG, monokine induced by interferon-γ ; IL, interleukin; EGF, epidermal growth factor; MIP, macrophage inflammatory protein; HGF, hepatocyte growth factor; VEGF, vascular endothelial growth factor; IFN-α,interferon alpha; MCP-1, macrophage chemoattractant peptide-1; FGF-2, basic fibroblast growth factor; IL-1RA, interleukin-1 receptor antagonist; IP10, interferon-γ -inducible protein 10; GM-CSF, granulocyte macrophage colony-stimulating factor; tumor necrosis factor-α (TNF-α), tumor necrosis factor alpha; RANTES, regulated on activation, normal T cell expressed and secreted
0.001), monokine induced by interferon-γ (MIG, P < 0.001), IL-2 (P < 0.001), IL-4 (P < 0.001), IL-6 (P = 0.032), IL-7 (P = 0.034), IL-5 (P = 0.044), and hepatocyte growth factor (HGF, P = 0.039), and significantly lower levels of epidermal growth factor (EGF, P = 0.006) and macrophage inflammatory protein-1α (MIP-1α, P = 0.02) in FEDF patients with SCZ compared with the controls (Table 1)
Summary
Schizophrenia (SCZ) is a severe mental disorder that has profound effects on society and affects individuals and families [1, 2]. The disease is characterized by hallucination, division of thinking, violent attacks, and delusion of victimization. It affects ∼1% of the population worldwide, with a male/female ratio of 1.4:1 [3]. Clinical and preclinical studies have indicated that miRNA dysregulation may play an etiological role in SCZ [4,5,6,7], and genome-wide significant association studies have identified hundreds of risk genes for SCZ [8,9,10]. Genetic studies have shown a correlation between genes that regulate the immune system and risk of SCZ; and immune dysfunction may be involved in the pathogenesis of SCZ in some individuals [10, 11]. Exploring the abnormalities in the immune system in patients with SCZ has attracted the attention of researchers in the field
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