Psychoneuroimmunolgy and Schizophrenia

Is there a connection between the immune system and psychiatric disorders?  Researchers in the field of psychoneuroimmunolgy have been able to determine that infections, which affect the immune system, have been linked to psychiatric disorders.  The immune system and the central nervous system (CNS) share the mechanisms of communication including chemical and electrical components known as neurotransmitters, neuropeptides, and cytokines.  Disregulation of the immune system is believed to contribute to the development of psychiatric disorders (Daruna, 2004).  Stress, infections, pathogens, toxins and other environmental factors are known to activate the immune system.   Some researchers believe that activation of certain immune system cells in response to an infection or on a chronic condition contributes to mental illness in different ways (Daruna).  Cytokines are small cell-signaling molecules that have been classified as proteins, peptides, or glycoproteins that are secreted by the innate and acquired immune systems.  They exert different effects on the targeted cell which can include inflammation, increase body temperature, respond to specific antigens and are responsible for growth and differentiation of cells within the immune system (Daruna).  Depression and distress enhance the production of proinflammatory cytokines.  Research suggests that there is a strong correlation between the immune system and the pathophysiology of schizophrenia (Strous & Shoenfeld, 2007).  Studies have demonstrated that patients with schizophrenia have non-specific over activation of the immunological response system, including T-helper cells, both Type 1 and Type 2 in the adaptive immune system (Steiner, 2010).  Type 1 T-helper cells promote the activation pro-inflammatory response.  Schizophrenic patients have also been found to have increased levels of cytokines, macrophages and lymphocytes in peripheral blood and bone marrow.  First psychotic break has been linked with immune system disregulation.  Researchers hypothesize that rapid changes occurring during adolescent brain development may trigger the activation of latent viruses or genes that create an immune response leading to the symptoms of first psychotic break (Daruna).  Patients with schizophrenia have demonstrated signs of neurodegeneration with progressive cortical atrophy.  Post-mortem analyses have confirmed the formation of lesions in the grey matter as well as elevated levels of the basic proteins that cause degeneration to human myelin.  Researchers have noted an increase incidence of schizophrenia with individuals born in the winter and in northern latitudes (Daruna).  Other studies suggest that in utero infections may be an underlying cause of schizophrenia (Meyer & Feldon, 2009).  Greater immunological disregulation is attributed to increased risk for the onset and acuity of schizophrenia (Daruna). 

References

Daruna, J. H.  (2004).  Introduction to Psychoneuroimmunology. Boston:  Elsevier Academic Press.

Meyer, U., & Feldon, J. (2009). Neural basis of psychosis-related behaviour in the infection model of schizophrenia. Behavioural Brain Research, 204(2), 322-334. doi:10.1016/j.bbr.2008.12.022

Steiner, J., Jacobs, R., Panteli, B., Brauner, M., Schiltz, K., Bahn, S., & ... Bogerts, B. (2010). Acute schizophrenia is accompanied by reduced T cell and increased B cell immunity. European Archives of Psychiatry & Clinical Neuroscience, 260(7), 509-518. doi:10.1007/s00406-010-0098-x

Strous, R. D., & Shoenfeld, Y. (2006). Schizophrenia, autoimmunity and immune system dysregulation: A comprehensive model updated and revisited. Journal of Autoimmunity, 27(2), 71-80. doi: 10.1016/j.jaut.2006.07.006