Article

The inflammatory response system in treatment-resistant schizophrenia: increased serum interleukin-6. Schizophr Res

Clinical Research Center for Mental Health (CRC-MH), University Department of Psychiatry, Antwerp, Belgium.
Schizophrenia Research (Impact Factor: 4.43). 07/1998; 32(1):9-15. DOI: 10.1016/S0920-9964(98)00034-6
Source: PubMed

ABSTRACT There is some evidence that the pathophysiology of schizophrenia is related to activation of the inflammatory response system (IRS), as indicated by increased serum concentrations of interleukin-6 (IL-6), IL-6 receptor (IL-6R), IL-1R antagonist (IL-1RA) and IL-2R and lower serum concentrations of CC16, an endogenous anti-inflammatory protein with immunosuppressive and anti-inflammatory effects. The aims of the present study were to examine serum CC16 in relation to IL-6, IL-6R and gp130, the IL-6 transducing signal protein, in schizophrenia and in treatment-resistant schizophrenia (TRS). Serum IL-6 and sIL-6R were significantly higher in medicated schizophrenic patients than in normal controls. Serum IL-6 was significantly higher in TRS than in normal volunteers, whereas schizophrenic patients without TRS showed intermediate values. Serum CC16 was significantly lower in schizophrenic patients with a positive family history for psychoses than in normal volunteers and patients without a positive family history. There was a significant inverse relationship between serum CC16 and serum IL-6 or sIL-6R in schizophrenic patients, but not in normal volunteers. The results suggest that the inflammatory response in schizophrenia, as indicated by increased serum IL-6 and sIL-6R, may be causally related to lower serum CC16 and that the latter might be a trait marker for schizophrenia.

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    • "Historically thought of as a culmination of 'a number of conditions which may lead to a severe disturbance of the ego',4) SCZ is now understood to arise from a complex interplay of genetic and environmental risk factors acting across many stages of brain development.5-11) Several neurochemical and neuropathological theories have been proposed to explain the pathological processes intrinsic to SCZ, including impairments in dopaminergic,12) glutamatergic13,14) and GABAergic signalling,15,16) impaired prefrontal cortex function,17-19) aberrant neurodevelopment, 11,20) stress vulnerability21) and variations in the inflammatory response.22,23) "
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    Clinical Psychopharmacology and Neuroscience 12/2013; 11(3):107-117. DOI:10.9758/cpn.2013.11.3.107
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