BACKGROUND: Increasing evidence indicates that childhood trauma is a risk factor for schizophrenia and patients with this syndrome have a pro-inflammatory phenotype. We tested the hypothesis that the pro-inflammatory phenotype in schizophrenia is associated with childhood trauma and that patients without a history of such trauma have a similar immune profile to healthy controls. METHOD: We recruited 40 schizophrenia patients and 40 controls, all of whom completed the Childhood Trauma Questionnaire (CTQ). Using enzyme-linked immunosorbent assay (ELISA) techniques, we measured peripheral levels of interleukin (IL)-1β, IL-6, IL-8 and tumour necrosis factor (TNF)-α. These immune parameters were compared in schizophrenia with childhood trauma, schizophrenia without childhood trauma and healthy controls. RESULTS: Patients with childhood trauma had higher levels of IL-6 and TNF-α than patients without trauma and healthy controls, and TNF-α levels correlated with the extent of the trauma. Patients with no trauma had similar immune profiles to controls. CONCLUSIONS: Childhood trauma drives changes, possibly epigenetic, that generate a pro-inflammatory phenotype.
BACKGROUND: Increasing evidence indicates that childhood trauma is a risk factor for schizophrenia and patients with this syndrome have a pro-inflammatory phenotype. We tested the hypothesis that the pro-inflammatory phenotype in schizophrenia is associated with childhood trauma and that patients without a history of such trauma have a similar immune profile to healthy controls. METHOD: We recruited 40 schizophreniapatients and 40 controls, all of whom completed the Childhood Trauma Questionnaire (CTQ). Using enzyme-linked immunosorbent assay (ELISA) techniques, we measured peripheral levels of interleukin (IL)-1β, IL-6, IL-8 and tumour necrosis factor (TNF)-α. These immune parameters were compared in schizophrenia with childhood trauma, schizophrenia without childhood trauma and healthy controls. RESULTS:Patients with childhood trauma had higher levels of IL-6 and TNF-α than patients without trauma and healthy controls, and TNF-α levels correlated with the extent of the trauma. Patients with no trauma had similar immune profiles to controls. CONCLUSIONS:Childhood trauma drives changes, possibly epigenetic, that generate a pro-inflammatory phenotype.
Authors: Tatiana Falcone; Damir Janigro; Rachel Lovell; Barry Simon; Charles A Brown; Mariela Herrera; Aye Mu Myint; Amit Anand Journal: J Psychiatr Res Date: 2014-12-25 Impact factor: 4.791
Authors: Suzi Hong; Ellen E Lee; Averria Sirkin Martin; Benchawanna Soontornniyomkij; Virawudh Soontornniyomkij; Cristian L Achim; Chase Reuter; Michael R Irwin; Lisa T Eyler; Dilip V Jeste Journal: Schizophr Res Date: 2016-09-17 Impact factor: 4.939