A psychoneuroimmunological review on cytokines involved in antidepressant treatment response

Abstract

Current literature demonstrates an association between antidepressant action and cytokine functioning in major depression. Improved understanding of the specific pharmacologic and pharmacogenetic mechanisms is needed. Such knowledge may serve to enhance our understanding of depression, leading to promising new directions in the pathology, nosology, and treatment of depression.

Bidirectional Prospective Associations of Metabolic Syndrome Components With Depression, Anxiety, and Antidepressant Use

“…This was particularly true for use of antidepressants, which compared with depressive and anxiety symptoms, negatively influenced a range of metabolic syndrome components after 2‐years. Antidepressants have pleiotropic effects across biological systems, including effects on autonomic nervous system, immune and inflammatory processes, oxidation, and cellular aging 53, 54, 55. These systems are all associated with negative consequences for cardiometabolic health and the development and maintenance cardiometabolic diseases 56, 57, 58.…”

Neuropharmacological evaluation of a novel 5-HT3 receptor antagonist (4-benzylpiperazin-1-yl)(3-methoxyquinoxalin-2-yl) methanone (6g) on lipopolysaccharide-induced anxiety models in mice

“…Oxidation of tryptophan is generally initiated by tryptophan dioxygenase enzyme, and negligibly by IDO enzyme. However, IDO is greatly increased by pro-inflammatory mediators such as cytokines, including TNF-α and IFN-γ [5,23,24]. Kynurenine pathway has important neuropsychiatric implications for the degradation of tryptophan [4].…”

Interaction Between Inflammatory State and Neurochemical Changes in Major Psychiatric Disorders

“…These findings resulted in clinical trials demonstrating the efficacy of non-steroidal anti-inflammatory drugs as add-on treatment of major depression (Müller et al, 2006;Akhondzadeh et al, 2009). On the other hand, antidepressants have significant anti-inflammatory effects, as recently reviewed by Janssen and colleagues (Janssen et al, 2010); they normalize elevated levels of circulating proinflammatory cytokines like IL-6, TNF-a, IFN-g, and IL-1, again indicating that the activation of the immune system may be directly involved in the pathophysiology of depression. Recent even demonstrate the possible usefulness of antidepressants to treat rheumatoid arthritis (Sacre et al, 2010).…”