Immuno-Psychiatry | 2021
Inflammation and Immunity in Schizophrenia
Abstract
This chapter presents evidence for a key role of inflammation in schizophrenia. In animal models, an immune response during the pre- or perinatal phase has been shown to affect lifelong immune function. Furthermore, levels of cytokines and other pro-inflammatory compounds are higher in people with schizophrenia than in healthy controls. Evidence from epidemiological and clinical studies shows that certain infections increase the risk for psychosis, in particular schizophrenia. The so-called vulnerability-stress-inflammation model has been proposed to explain how inflammation is involved in schizophrenia. According to this model, schizophrenia is related to risk genes for inflammation, alterations in the immune system, and exposure to environmental stress factors. Stress is known to increase cytokine levels and may play a role in a chronic proinflammatory state. The proposed involvement of low-level neuroinflammation in schizophrenia is supported by several findings: altered neurotransmission is a typical feature of both neuroinflammation and schizophrenia; patients with schizophrenia have a loss of volume in central nervous system structures and activated microglia; anti-inflammatory drugs have positive effects in schizophrenia; and antipsychotics have anti-inflammatory and immunomodulatory effects. Together, these findings indicate that the immune system may be a potential target for novel treatments for schizophrenia.