F23. LOW-GRADE INFLAMMATORY PROFILE IN FIRST-EPISODE PSYCHOSIS: RESULTS FROM THE STREAM STUDY IN BRAZIL.

AbstractBackgroundThe inflammatory hypothesis of schizophrenia suggests that abnormalities in inflammatory factors may contribute to the onset of this disease early in adulthood. Nevertheless, no study has investigated possible effects of shared environment by looking at cytokine levels in healthy siblings of first-episode psychosis patients (FEP). The aim of this study was to investigate inflammatory cytokine (IL-6, IL-10, TNF-a) abnormalities in a sizeable epidemiological-based sample of FEP patients, their healthy siblings and population-based controls.MethodsThis study is part of the epidemiological investigation “Schizophrenia and Other Psychoses Translational Research: Environment and Molecular Biology” (STREAM), conducted in Ribeirao Preto (Sao Paulo, Brazil) and surrounding area, which is part of the international consortium “European Network of National Schizophrenia Networks Studying Gene-Environment Interactions” (EU-GEI). We recruited a total sample of 507 participants, composed by 166 FEP patients (64% males; mean age: 30.3 ± 12.2), 76 siblings (30.3% males; mean age: 31.5 ± 11.0) and 265 population-based controls (50.2% males; mean age: 31.7 ± 11.2). Plasma cytokines IL-6, TNF-a and IL-10 were analysed by Multiplex Bead Array (Luminex xMap technology). We performed the multivariate general linear model (GLM) analysis with age as covariate, cytokines as dependent variables and diagnostic group and sex as explanatory variables.ResultsWe found significant differences between the three groups [F (6,994) = 10.864; p 0.05 for all).DiscussionThis is the first study conducted in the South hemisphere to demonstrate the low-grade inflammatory profile in FEP patients, compared to their siblings and community-based controls. The fact that IL-6, TNF-a and IL-10 are all higher in the FEP group than their healthy siblings and community-based controls suggests the synergism of individual vulnerability factors in the development of this inflammatory profile.