Cytokine levels in major depression are related to childhood trauma but not to recent stressors

Grosse, Laura; Ambrée, Oliver; Jörgens, Silke; Jawahar, Magdalene C.; Singhal, Gaurav; Stacey, David; Arolt, Volker; Baune, Bernhard T.

doi:10.1016/j.psyneuen.2016.07.205

Cited by 84 publications

(48 citation statements)

References 27 publications

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“…Tumor necrosis factor is a proinflammatory cytokine; it can induce fever, apoptotic cell death, and inflammation. 16 Apart from playing roles in the pathogenesis of IBD, deregulation of TNF is also found in other diseases, such as Alzheimer disease, 17 major depression, 18 and psoriasis. 19 The present data reveal a novel aspect of TNF that TNF also interferes with the expression of IL-10 in peripheral B cells.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor suppresses interleukin 10 in peripheral B cells via upregulating Bcl2‐like protein 12 in patients with inflammatory bowel disease

Guo

et al. 2017

Cell Biochemistry & Function

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The pathogenesis of the immune regulation dysfunction is unclear. Bcl2-like protein 12 (Bcl2L12) has immune suppression function. This study tests a hypothesis that tumor necrosis factor (TNF) increases Bcl2L12 to suppress the expression of interleukin (IL) 10 in peripheral B cells of patients with inflammatory bowel disease (IBD). In this study, peripheral blood samples were collected from IBD patients and healthy controls. B cells were isolated from the blood samples. The expression of IL-10 and Bcl2L12 in B cells was analyzed by quantitative reverse transcription polymerase chain reaction and Western blotting. We observed that the expression of Bcl2L12 in the peripheral B cells was higher in IBD patients than that in healthy controls. The IL-10 levels in B cells were negatively correlated with the expression of Bcl2L12. Exposure of B cells to TNF in the culture enhanced the expression of Bcl2L12. The Bcl2L12 mediated the effects of TNF on suppression of IL-10 in B cells. In conclusion, Bcl2L12 mediates the effects of TNF to suppress the expression of IL-10 in B cells. The data suggest that Bcl2L12 may be a therapeutic target for the treatment of IBD.

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Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor suppresses interleukin 10 in peripheral B cells via upregulating Bcl2‐like protein 12 in patients with inflammatory bowel disease

Guo

et al. 2017

Cell Biochemistry & Function

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“…The presence of increased immune activation in patients with psychiatric disorders across different diagnostic categories has generated increasing interest in unravelling causes behind this immune activation. In the context of peripheral immune activation, several clinical studies so far have shown that inflammatory markers, such as IL-6 and CRP, are particularly high in patients who had experienced childhood traumatic events, including physical or sexual abuse, emotional abuse or neglect that occur in childhood; this has been demonstrated in patients suffering with psychosis, major depression or bipolar disorder [9][10][11][12][13]. These primary research findings are supported by evidence from systematic reviews that provide evidence for prolonged peripheral inflammation following exposure to traumatic events in childhood [8,11,14].…”

Section: Increased Circulating Cytokines and Acute-phase Proteinsmentioning

confidence: 99%

From early adversities to immune activation in psychiatric disorders: the role of the sympathetic nervous system

Mondelli

Vernon

2019

Clinical and Experimental Immunology

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Summary Increased peripheral levels of cytokines and central microglial activation have been reported in patients with psychiatric disorders. The degree of both innate and adaptive immune activation is also associated with worse clinical outcomes and poor treatment response in these patients. Understanding the possible causes and mechanisms leading to this immune activation is therefore an important and necessary step for the development of novel and more effective treatment strategies for these patients. In this work, we review the evidence of literature pointing to childhood trauma as one of the main causes behind the increased immune activation in patients with psychiatric disorders. We then discuss the potential mechanisms linking the experience of early life adversity (ELA) to innate immune activation. Specifically, we focus on the innervation of the bone marrow from sympathetic nervous system (SNS) as a new and emerging mechanism that has the potential to bridge the observed increases in both central and peripheral inflammatory markers in patients exposed to ELA. Experimental studies in laboratory rodents suggest that SNS activation following early life stress exposure causes a shift in the profile of innate immune cells, with an increase in proinflammatory monocytes. In turn, these cells traffic to the brain and influence neural circuitry, which manifests as increased anxiety and other relevant behavioural phenotypes. To date, however, very few studies have been conducted to explore this candidate mechanism in humans. Future research is also needed to clarify whether these pathways could be partially reversible to improve prevention and treatment strategies in the future.

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“…It has been suggested that TRD patients might have distinct characteristics from non-TRD patients (Kornstein and Schneider, 2001), and indirect evidence that dysregulated inflammatory activity may be a distinguishing feature (Raison et al, 2013;Strawbridge et al, 2018). Heightened inflammation might even represent a common link between treatment resistance and other core elements of TRD, such as physical illness or poor physical health (Maes et al, 2011), chronicity and/or recurrence of depressive illness (Anisman et al, 1999), cognitive impairments (Li et al, 2018) or early life trauma (Grosse et al, 2016). However, these factors are rarely assessed concurrently.…”

Section: Accepted Manuscript Introductionmentioning

confidence: 99%

Inflammatory profiles of severe treatment-resistant depression

Strawbridge

Hodsoll

Powell

et al. 2019

Journal of Affective Disorders

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Cytokine levels in major depression are related to childhood trauma but not to recent stressors

Cited by 84 publications

References 27 publications

Tumor necrosis factor suppresses interleukin 10 in peripheral B cells via upregulating Bcl2‐like protein 12 in patients with inflammatory bowel disease

Tumor necrosis factor suppresses interleukin 10 in peripheral B cells via upregulating Bcl2‐like protein 12 in patients with inflammatory bowel disease

From early adversities to immune activation in psychiatric disorders: the role of the sympathetic nervous system

Inflammatory profiles of severe treatment-resistant depression

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