The inflammatory response system activation model of major depression

Abstract

The present paper proposes a concise inflammatory response system (IRS)- activation model of major depression. The evidence that alterations in the 1RS participate in the pathophysiology or even etiology of major depression consists of the following. 1) Confirmed findings of in vivo 1RS activation in major depression, such as increased numbers of leukocytes, monocytes, neutrophils, activated T-lymphocytes, increased secretion of neopterin and prostaglandins, and increased secretion of proinflammatory cytokines, such as interleukin-lβ (IL-lβ), IL-6 and interferon-γ (IFNγ). 2) A variety of antidepressants, such as selective serotonin reuptake inhibitors and tricyclic antidepressants, have negative immunoregulatory activities. 3) Activation of the 1RS in major depression is significantly related to some of the neuroendocrine disorders in that illness. 4) Proinflammatory cytokines, such as IL-1, IL-6 and interferons given to humans or animals can produce depressive symptoms or full blown major depression. 5) The 1RS activation model may account for the multicausal etiology of major depression whereby external or psychosocial Stressors (negative life events), and internal or organic Stressors are considered to play a pivotal role in the etiology of depression.