Levels of certain cytokines are altered in patients with first-episode psychosis (FEP) and patients with schizophrenia, research shows.
Milica Borovcanin (University of Kragujevac, Serbia) and team found that serum levels of interleukin (IL)-17, the type-2 immune response cytokine IL-4, and the regulatory cytokine transforming growth factor (TGF)-β are altered in FEP and relapsed schizophrenia patients compared with controls.
In total, 88 antipsychotic-naive FEP patients, 45 relapsed schizophrenia patients, and 36 mentally healthy controls participated in the study. There were no significant differences among the groups regarding gender distribution and age.
Blood samples were collected from all of the participants and assessed for levels of IL-17, the type-1 cytokines tumor necrosis factor-α and interferon-γ, the type-2 cytokines IL-4 and IL-10, and the regulatory cytokines TGF-β, IL-27, and IL-6.
The team found that mean levels of IL-17 were significantly reduced in both groups of psychotic patients combined compared with controls, at 21.13 versus 30.86 pg/mL.
By contrast, mean levels of IL-4 were increased in both groups of psychotic patients compared with controls, at 27.12 versus 12.09 pg/mL.
Among the psychotic patients, those with schizophrenia had significantly higher IL-4 levels than FEP patient, at 30.70 versus 25.10 pg/mL.
In addition, schizophrenia and FEP patients had significantly higher levels of TGF-β compared with controls, at 72.57 and 49.83 versus 21.23 pg/mL, respectively. The difference between the two patient groups was not significant.
Borovcanin et al summarize: "In our study we have demonstrated that type-1 and type-17 responses are blunted and type-2 [responses] overweight in schizophrenia. Also, we have presented [an] increase in systemic production of TGF-β and decreased serum levels of IL-17 in psychotic patients."
They conclude in the Journal of Psychiatric Research: "The presence of enhanced anti-inflammatory/immunosuppressive activity in schizophrenia may be an attempt to counteract or limit ongoing pro-inflammatory processes and [downregulate] chronic inflammation."
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