The inflammatory response system activation model of major depression

The present paper proposes a concise inflammatory response system (IRS)acti vation model of major depression. The evidence that alterations in the IRS participate in the pathophysiology or even etiology of major depression con sists of the following. 1) Confirmed findings of in vivo IRS activation in major depression, such as increased numbers of leukocytes, monocytes, neutr ophils, activated T-lymphocytes, increased secretion of neopterin and prost aglandins, and increased secretion of proinflammatory cytokines, such as in terleukin-1 beta (IL-1 beta), IL-6 and interferon-gamma (IFN gamma). 2) A v ariety of antidepressants, such as selective serotonin reuptake inhibitors and tricyclic antidepressants, have negative immunoregulatory activities. 3 ) Activation of the IRS in major depression is significantly related to som e of the neuroendocrine disorders in that illness. 4) Proinflammatory cytok ines, such as IL-1, IL-6 and interferons given to humans or animals can pro duce depressive symptoms or full blown major depression. 5) The IRS activat ion model may account for the multicausal etiology of major depression wher eby external or psychosocial stressors (negative life events), and internal or organic stressors are considered to play a pivotal role in the etiology of depression.