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Schizophr Res. 1997 Aug 29;26(2-3):227-33.

A differential role for interleukin-6 and tumor necrosis factor-alpha in schizophrenia?

Author information

1
Service Hospitalo-Universitaire de Psychiatrie, CHU Sainte-Marguerite, Marseille, France. artsnaud@pacwan.mm-soft.fr

Abstract

Pro-inflammatory cytokines are dysregulated in schizophrenia. To determine the nature of the so-called inflammatory syndrome in schizophrenia, we investigated the circulating levels of various cytokines (interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)alpha), their natural antagonist (IL1-ra, TNF-RI, TNF-RII) and leukocyte activation markers (the soluble receptor of interleukin-2, soluble CD14 and soluble CD23) in subjects with chronic schizophrenia (n = 18) and in normal controls (n = 21). The levels of IL-1 beta and its antagonist and the levels of leukocyte activation markers were not significantly differents between patients and controls. Circulating levels of TNF alpha were significantly (p < 0.05) higher in patients than in controls and did not result from variations of its antagonist levels. The significant (p < 0.05) increase in patient IL-6 was related specifically to clinical status, i.e. illness duration. These data suggest a specific cytokine-mediated syndrome in schizophrenia. We hypothesize that TNF alpha and IL-6 reflect the genetic background of disease suceptibility.

PMID:
9323355
[Indexed for MEDLINE]

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