Aim. To present the role of immunoactivation associated with pro-inflammatory and neurodegenerative processes in the onset of depression symptoms.
Review. In depressed patients without any concurrent pro-inflammatory disease of known etiology, increased levels of pro-inflammatory cytokines and other markers of inflammatory process are observed. On the other hand, increased susceptibility to depression has been reported in patients with an elevated serum level of pro-inflammatory cytokines resulting from on-going inflammatory processes (e.g. rheumatoid arthritis). Psychological stress leads to an increase in the production of pro-inflammatory cytokines and at the same time may contribute to the development of depressive symptoms. Immunotherapy using pro-inflammatory cytokines of some neoplastic diseases and chronic type C hepatitis results in depressive states. Administration of pro-inflammatory cytokines or lipopolysaccharide (which activates cytokine secretion) to laboratory animals evokes a state resembling depression. In neuroimaging studies the same changes in the activity of cerebral structures have been found in depressed patients and in those receiving cytokine immunotherapy. Antidepressants eliminate depressive states induced by the administration of pro-inflammatory cytokines, and besides, inhibit the synthesis of pro-inflammatory cytokines in vitro. The latter findings confirm the role of cytokines in the onset of depression and suggest that therapeutic action of these drugs may be connected with their immunosuppressive effect.