Role of inflammatory cytokines in depression: Focus on interleukin-1β

Abstract

Abstract. According to the World Health Organization, major depression will become the leading cause of disability worldwide by the year 2030. Despite extensive research into the mechanisms underlying this disease, the rate, prevalence and disease burden has been on the rise, particularly in the industrialized world. Epidemiological studies have shown biological and biochemical differences in disease characteristics and treatment responses in different age groups. Notable differences have been observed in the clinical presentation, co-prevalence with other diseases, interaction with the immune system and even in the outcome. Thus, there is an increased interest in characterizing these differences, particularly in terms of contribution of different factors, including age, cytokines and immunotherapy. Research into the possible mechanisms of these interactions may reveal novel opportunities for future pharmacotherapy. The aim of the present review is to document recent literature regarding the impact of inflammatory mechanisms on the pathophysiology of the depressive disorder.

Brain inflammasomes in stroke and depressive disorders: Regulation by oestrogen

“…Interestingly, n‐3 PUFA supplementation decreased hippocampal IL‐1β expression only in rats injected simultaneously with E 2 . Taken together, these reports clearly suggest a participation of inflammatory cytokines, their metabolic enzymes and molecular inducers in the aetiology of neuropsychiatric illness, with a particular emphasis on MD and a potential regulatory function of E 2 …”

“…Besides the genetic and epigenetic factors involved in the prevalence, course and severity of MD, disturbed neuroimmune functions and reciprocal neurone‐microglia interactions are discussed either as consequences of this mental disease or causes . Neuroinflammation and inflammatory cytokines/chemokines affect brain signal patterns involved in the psychopathology of MD . Women are more prone to depression, with a two‐fold higher lifetime risk of developing MD compared to men, and women′s symptoms determined by multiple depression scales are more severe than men .…”

“…62,63 Neuroinflammation and inflammatory cytokines/chemokines affect brain signal patterns involved in the psychopathology of MD. 62,64 Women are more prone to depression, with a two-fold higher lifetime risk of developing MD compared to men, and women′s symptoms determined by multiple depression scales are more severe than men. 65 This implicates the participation of female sex steroids in the genesis and/or course of MD.…”

“…Taken together, these reports clearly suggest a participation of inflammatory cytokines, their metabolic enzymes and molecular inducers in the aetiology of neuropsychiatric illness, with a particular emphasis on MD and a potential regulatory function of E 2 . 62,64,81 The question arises as to whether these effects of E 2 can be traced to the inflammasome signalling platform. Only sparse data regarding this issue have been reported.…”

Biomarkers for Depression: Recent Insights, Current Challenges and Future Prospects

“…40 IL-1β is even more inconclusively associated with depression, with meta-analyses suggesting higher levels in depression (P=0.03), 41 high levels only in European studies 42 or no differences from controls. 40 Despite this, a recent article suggested particular translational implications for IL-1β, 44 supported by an extremely significant effect of elevated IL-1β ribonucleic acid predicting a poor response to antidepressants; 45 other findings above pertain to circulating blood-derived cytokines. The chemokine monocyte chemoattractant protein-1 has shown elevations in depressed participants in one meta-analysis.…”