Indoleamine 2,3-dioxygenase and immune changes under antidepressive treatment in major depression in females.
نویسندگان
چکیده
BACKGROUND/AIM Indoleamine 2, 3-dioxygenase (IDO) induction has been suggested as a mechanism by which immune activation affects tryptophan metabolism and serotonin synthesis in major depressive disorder (MDD). We investigated IDO and changes in inflammatory mediators in patients with MDD undergoing effective treatment. PATIENTS AND METHODS Forty female patients with MDD and 40 controls were recruited. Serum IDO was assessed by enzyme-linked immunosorbent assay (ELISA). We also determined tumor necrosis factor-α (TNFα), interferon-γ (IFNγ), C-reactive protein (CRP) and serotonin concentrations. RESULTS Patients' baseline concentrations of IDO and immune mediators were higher and serotonin concentrations were lower compared to controls. IDO and TNFα concentrations decreased under treatment and IDO changes were positively correlated with patient improvement. IFNγ and CRP concentrations remained unchanged. Serotonin concentration tended to increase. CONCLUSION IDO might play an important role in the pathophysiology of MDD. Moreover, antidepressant therapy might reduce IDO production through an IFNγ-independent pathway. Finally, peripheral concentration of IDO assessed by ELISA might be a useful marker of MDD.
منابع مشابه
A biological pathway linking inflammation and depression: activation of indoleamine 2,3-dioxygenase
This article highlights the evidence linking depression to increased inflammatory drive and explores putative mechanisms for the association by reviewing both preclinical and clinical literature. The enzyme indoleamine 2,3-dioxygenase is induced by proinflammatory cytokines and may form a link between immune functioning and altered neurotransmission, which results in depression. Increased indol...
متن کاملImmunological aspects of the treatment of depression and schizophrenia
Schizophrenia and major depression (MD) have been associated with immune system dysfunction. One example of this is the altered level of cytokines-important inflammatory mediators-in blood, and a proinflammatory immune state has been described in some subgroups of patients. A knock to the immune system in early life might trigger a life-long increased immune reactivity, and infections and autoi...
متن کاملIndoleamine 2,3-Dioxygenase and Immunological Tolerance during Pregnancy
Indoleamine 2,3-dioxygenase (IDO), an enzyme involved in the catabolism of tryptophan, is expressed by a variety of cells and tissues such as macrophages, dendritic cells, cells of the endocrine system and by the placenta. IFN- γ is the main inducer of this enzyme. IDO acts as an important defense mechanism of innate immunity against pathogens. It also has tumor suppressive activity and prolong...
متن کاملThe TNF-alpha inhibitor etanercept as monotherapy in treatment-resistant depression - report of two cases.
Growing evidence links affective disorders and the immune system. Pro-inflammatory cytokines are implicated in the pathogenesis of depression by activation of the tryptophanand serotonin-degrading enzyme indolamine-2,3-dioxygenase (IDO) (Kiank et al. 2010) and by up-regulating serotonin transporter activity (Zhu et al. 2006), leading to reduced availability of serotonin. Pro-inflammatory cytoki...
متن کاملStress, the Autonomic Nervous System, and the Immune-kynurenine Pathway in the Etiology of Depression
The autonomic nervous system is one of the major neural pathways activated by stress. In situations that are often associated with chronic stress, such as major depressive disorder, the sympathetic nervous system can be continuously activated without the normal counteraction of the parasympathetic nervous system. As a result, the immune system can be activated with increased levels of pro-infla...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- In vivo
دوره 28 4 شماره
صفحات -
تاریخ انتشار 2014