NLRP3 inflammasome is activated in mononuclear blood cells from patients with major depressive disorder

Alcocer-Gómez, Elísabet; Miguel, Manuel de; Barquero, N. Casas; Núñez-Vasco, Jéssica; Sánchez-Alcázar, José A.; Fernández-Rodríguez, Ana; Cordero, Mario D.

doi:10.1016/j.bbi.2013.10.017

Cited by 364 publications

(278 citation statements)

References 37 publications

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“…In addition, chronic corticosterone treatment that mimics stress increased NLRP3 levels in the hippocampus . The recent findings of increased levels of NLRP3 and active caspase-1 in mononuclear blood cells from patients with major depression (Alcocer-Gómez et al, 2014) indicate that activation of the NLRP3 inflammasome contributes to inflammation that is known to be associated with depression Miller et al, 2009;Kubera et al, 2011;Zunszain et al, 2013). We found that NLRP3 and p20 active caspase-1 increased 24 hr after acute stress in the hippocampus.…”

Section: Discussionsupporting

confidence: 54%

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Cheng

Jope

Beurel

2016

Psychoneuroendocrinology

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Section: Discussionsupporting

confidence: 54%

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Cheng

Jope

Beurel

2016

Psychoneuroendocrinology

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“…Under stimulation and stress, the NLRP3 inflammasome complex induces the cleavage and activation of caspase-1, which promotes the maturation of IL-1β (7). A previous study reported that activated NLRP3 inflammasome along with increased serum levels of IL-1β and IL-18 were observed in mononuclear blood cells from patients with major depressive disorder (8). Furthermore, the NLRP3 inflammasome was demonstrated to mediate IL-1 β-associated central nervous system (CNS) inflammation in animal models of stress-induced depression (9,10).…”

Section: Introductionmentioning

confidence: 99%

Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress

Gao

Zhu

et al. 2017

Exp Ther Med

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Abstract. Atractylenolide I (AT-I), a major component of the rhizoma of Atractylodes macrocephala Koidz., exerts a wide range of activities. The purpose of the present study was to investigate the anti-depressant-like effect of AT-I in a mouse model of chronic unpredictable mild stress (CUMS), and to explore the possible molecular mechanism involved. It was revealed that AT-I significantly ameliorated CUMS-induced depressive-like behaviors, as evidenced by increased sucrose preference as well as shortened immobility time in the forced swimming and the tail suspension test. In addition, AT-I reduced CUMS-induced decreases in the concentrations of serotonin and norepinephrine in the hippocampus. Furthermore, AT-I inhibited the activation of the nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome as well as the concentration of the pro-inflammatory cytokine interleukin (IL)-1β in the hippocampi of mice subjected to CUMS. In conclusion, the results of the present study suggested that AT-I exerts anti-depressant-like effects in a CUMS-induced model of depression in mice, the molecular mechanism of which is associated with the inhibition of NLRP3 inflammasome activation to decrease IL-1β production.

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“…In addition, there is evidence of activation of the NLRP3 inflammasome in patients with MDD (Alcocer-Gomez and Cordero, 2014a; Drago et al, 2015). Specifically, patients with depression had increased expression of NLRP3 and caspase-1 in peripheral blood mononuclear cells (Alcocer-Gomez et al (2014b)). Thus, sterile inflammation mediated by DAMPs and the inflammasome and evoked after exposure to psychological stressors may have a role in the pathogenesis of MDDs and other psychopathologies (Alcocer-Gomez and Cordero, 2014a; Kessler, 1997;Miller et al, 2015).…”

Section: Stress Damps and Sterile Inflammationmentioning

confidence: 99%

Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders

Fleshner

Frank

Maier

2016

Neuropsychopharmacol

183

125

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Major depressive disorder (MDD) and other mood disorders remain difficult to effectively treat, and innovative interventions and therapeutic targets are needed. Psychological stressors and inappropriate inflammation increase the risk and severity of mood disorders; however, only recently have the importance of sterile inflammatory processes in this effect been revealed. This review will introduce the reader to pathogen vs sterile inflammation, inflammatory receptor-ligand interactions, microbialassociated molecular patterns (MAMPs), pathogen-associated molecular patterns (PAMPs), danger-associated molecular patterns (DAMPs), and the more recent discovery of the role of the inflammasome in peripheral and central nervous system cytokine/chemokine inflammatory responses. The review will focus on current preclinical and clinical evidence that sterile inflammation and inflammasome-dependent signaling may contribute to mood disorders. By understanding these inflammatory signaling processes, new approaches for quieting chronic or inappropriate inflammatory states may be revealed and this could serve as novel pharmacological targets for the treatment of mood disorders.

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NLRP3 inflammasome is activated in mononuclear blood cells from patients with major depressive disorder

Cited by 364 publications

References 37 publications

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress

Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders

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