Inflammatory cytokine-associated depression

Abstract

Inflammatory cytokines can sometimes trigger depression in humans, are often associated with depression, and can elicit some behaviors in animals that are homologous to major depression. Moreover, these cytokines can affect monoaminergic and glutamatergic systems, supporting an overlapping pathoetiology with major depression. This suggests that there could be a specific major depression subtype, inflammatory cytokine-associated depression (ICAD), which may require different therapeutic approaches. However, most people do not develop depression, even when exposed to sustained elevations in inflammatory cytokines. Thus several vulnerabilities and sources of resilience to inflammation-associated depression have been identified. These range from genetic differences in neurotrophic and serotonergic systems to sleep quality and omega-3 fatty acid levels. Replicating these sources of resilience as treatments could be one approach for preventing “ICAD”.

Impact of Serum Cytokine Levels on EEG-Measured Arousal Regulation in Patients with Major Depressive Disorder and Healthy Controls

“…In depression, proinflammatory cytokines were found to interact with the HPA axis, to stimulate the serotonin-depleting indolamine-2,3-dioxygenase and to trigger serotonin reuptake [6,8,9]. Levels of proinflammatory cytokines were repeatedly found to be elevated in depressed patients as well as in animal models of depression [6,10,11], potentially representing an inflammation-associated specific subtype of MDD [12,13,14] and a target for new antidepressant treatment strategies [15,16]. …”

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities

“…Persistent low-grade immune-inflammatory processes are an integral part of the pathophysiology of a substantial subset of patients with major depressive disorder (MDD) [1,2] . Among various immune-inflammatory marker elevations in MDD, meta-analytic evidence indicates that peripheral levels of interleukin (IL)-1β, IL-6, C-reactive protein (CRP), and soluble IL-2 receptor (sIL-2R) are higher in individuals with MDD compared to healthy controls [3,4] .…”

Poly (ADP-ribose) polymerase-1 inhibitor, 3-aminobenzamide pretreatment ameliorates lipopolysaccharide-induced neurobehavioral and neurochemical anomalies in mice

“…Precedent preclinical and clinical studies imply that the development of depressive disorders is connected with an unrelenting activation of the innate immune system and inflammatory processes (Goshen et al, 2008;Dowlati et al, 2010;Patki et al, 2013;Zeugmann et al, 2013;Lotrich., 2014). Raised levels of IL-1β, IL-6 and TNF-α is generally observed in many preclinical depression models (Gibney et al, 2013;Karlović et al, 2012;Rizzo et al, 2012).…”