Abstract
Glial damage and immune dysfunction are involved in pathogenesis of schizophrenia. However, interaction between glial damage and immune dysfunction in schizophrenia is undefined. This study aims to compare plasma S100 calcium binding protein (S100B) levels between schizophrenia patients and healthy participants, and to determine if immune markers are independently related with concentration of S100B in schizophrenia patients. Forty-one schizophrenia patients and thirty-three healthy volunteers were enrolled. Enzyme-linked immunosorbent assay (ELISA) was used to assess the concentrations of plasma S100B and inflammatory markers. We found that concentrations of S100B were elevated in schizophrenia patients than healthy participants (p < 0.05), and were negatively related with the severity of symptoms (p = 0.046). Receiver operating characteristic (ROC) curve analysis showed that different S100B levels between schizophrenia and healthy participants can be used as a clinical diagnostic factor (predictive value: 0.666, p = 0.015). Multiple linear regression analysis found that length of illness (Beta = −0.161), plasma levels of inflammatory regulation factors (including TGF-β1, logIL-23 and logIL-10) (Beta = 0.119, 0.475, 0.514) were independently associated with concentrations of S100B (Adjusted R2 = 0.897, p < 0.001). Therefore, our results suggest the possible function of S100B in pathogenesis of schizophrenia, and implicate the important role of autoimmune response and balance to glial dysfunction in patients with schizophrenia.
Highlights
During the past two decades, the associations between brain tissue damage, or glial cell dysfunction and schizophrenia have been repeatedly reported[4,5]
The Binary logistic regression test after adjusting to age, sex, education level, marital status showed there is a direct effect of logS100B with schizophrenia (P = 0.019, odds ratio = 10.599; 95% confidence interval = 1.477–76.049)
Our finding is consistent with the results of numerous previous studies, which consistently found increased concentrations of S100 calcium binding protein (S100B) in blood of patients with schizophrenia[4,10,11,35,36], some contravariant reports[14,37]
Summary
During the past two decades, the associations between brain tissue damage, or glial cell dysfunction (astrocytes and oligodendrocytes) and schizophrenia have been repeatedly reported[4,5]. Rothermundt et al found that levels of S100B were positively correlated with negative symptomatology, but Schmitt et al found that levels of S100B were negatively correlated with deficit symptoms[15,20], and some studies found no correlation[14]. During these decades, numerous studies from different areas showed that immune dysfunction was related with central neural system, and involved in the pathogenesis of schizophrenia[21]. Seki found that aripiprazole, an atypical antipsychotic, suppresses the TNF-αsecretion from interferon-γactivated microglia and inhibits the apoptosis of rodent oligodendrocytes by interferon-γactivated microglia[32]
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