The effects of early life adversity on the immune system

Elwenspoek, Martha M C; Kuehn, Annette; Muller, Claude P.; Turner, Jonathan D.

doi:10.1016/j.psyneuen.2017.05.012

Cited by 151 publications

(112 citation statements)

References 164 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Besides the immunoenhancing effects of these severe early-life stressors, also comparatively mild stressors, such as low childhood SES, indicated by socioeconomic conditions such as a lack of home ownership or low parental education, were significant predictors of inflammatory potential in adulthood, as evidenced by increased expression of inflammatory genes in circulating immune cells [280, 282] and increased plasma IL-6 and CRP concentrations [312]. In line with the latter and findings reported above for women with a history of childhood maltreatment, three other studies found exaggerated IL-6 responses to ex vivo stimulation of toll-like receptors 3, 4, and 5 in adolescents raised in harsh family environments [281], in adults raised in low socioeconomic status [282], and in adolescent girls with early-life adversity [107, 112]. Reports of severe adversity in the form of documented abuse were further associated with a 73% greater risk of first hospital treatment of asthma and more frequent asthma-related hospitalizations [144, 216].…”

Section: Stress Inflammation and Mental Health: The Cytokine Theorysupporting

confidence: 55%

“…Independent of facing additional social stressors, spontaneous production of proinflammatory cytokines in isolated immune cells was also higher in women with a history of childhood maltreatment [40]. Three other studies further found exaggerated IL-6 responses to ex vivo stimulation of toll-like receptors 3, 4, and 5 in adolescents raised in harsh family environments [281], in adults raised in low socioeconomic status [282] and in adolescent girls with early-life adversity [107, 112]. These human data are in line with work done by our group and others, demonstrating increased immune (re-)activity [27, 401, 406], anxiety-related behavior [348, 405], and psychosocial stress vulnerability [406] in adult rodents exposed to maternal separation from postnatal days 1–14, an internationally accepted animal model for early-life stress/trauma [149, 159, 175, 184, 209, 297, 322, 360, 404, 422].…”

Section: Stress Inflammation and Mental Health: The Cytokine Theorymentioning

confidence: 99%

See 1 more Smart Citation

Old Friends, immunoregulation, and stress resilience

Langgartner

Lowry

Reber³

2018

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

There is a considerable body of evidence indicating that chronic adverse experience, especially chronic psychosocial stress/trauma, represents a major risk factor for the development of many somatic and affective disorders, including inflammatory bowel disease (IBD) and posttraumatic stress disorder (PTSD). However, the mechanisms underlying the development of chronic stress-associated disorders are still in large part unknown, and current treatment and prevention strategies lack efficacy and reliability. A greater understanding of mechanisms involved in the development and persistence of chronic stress-induced disorders may lead to novel approaches to prevention and treatment of these disorders. In this review, we provide evidence indicating that increases in immune (re-)activity and inflammation, potentially promoted by a reduced exposure to immunoregulatory microorganisms (“Old Friends”) in today’s modern society, may be causal factors in mediating the vulnerability to development and persistence of stress-related pathologies. Moreover, we discuss strategies to increase immunoregulatory processes and attenuate inflammation, as for instance contact with immunoregulatory Old Friends, which appears to be a promising strategy to promote stress resilience and to prevent/treat chronic stress-related disorders.

show abstract

Section: Stress Inflammation and Mental Health: The Cytokine Theorysupporting

confidence: 55%

Section: Stress Inflammation and Mental Health: The Cytokine Theorymentioning

confidence: 99%

Old Friends, immunoregulation, and stress resilience

Langgartner

Lowry

Reber³

2018

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

show abstract

“…Collectively, these results suggest that ELA exposure is associated with a sustained activation of adaptive immunity and accelerated immune ageing, as indexed by the increase in T cell senescence. These effects appeared to be independent of either stress or health‐risk behaviours, suggestive of a primary effect of early life programming on specific immune cell populations . Exploring how social adversity may affect peripheral immune cells, Counotte et al .…”

Section: Evidence For the Association Between Ela And Activation Of Tmentioning

confidence: 98%

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

Mondelli

Vernon

2019

Clinical and Experimental Immunology

View full text Add to dashboard Cite

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.

show abstract

“…ELS is associated with an immune phenotype characterized by increased inflammation, impaired cell‐mediated immune responses, and premature immunosenescence . Higher basal or stress‐induced levels of plasma cytokines, including IL‐6, IL‐1β, and serum TNF‐α, have been described in healthy adults exposed to ELS .…”

Section: Early‐life Stress Leads To Chronic Inflammationmentioning

confidence: 99%

“…Large epidemiological cohorts reported that ELS is an independent risk factor for inflammation later in life . The current literature suggests that ELS accelerates telomere attrition in peripheral PBMCs, as well as leading to the accumulation of age‐related epigenetic changes . Although it is well established that adults with ELS have immune changes associated with cellular activation and inflammation, it is largely unknown whether these changes precede the onset of neuropsychiatric disorders.…”

Section: Early‐life Stress Leads To Chronic Inflammationmentioning

confidence: 99%

Inflammation in psychiatric disorders: what comes first?

Bauer

Teixeira

2018

Annals of the New York Academy of Sciences

344

208

View full text Add to dashboard Cite

Neuropsychiatric disorders (i.e., mood disorders and schizophrenia) and inflammation are closely intertwined, and possibly powering each other in a bidirectional loop. Depression facilitates inflammatory reactions and inflammation promotes depression and other neuropsychiatric disorders. Patients with neuropsychiatric disorders exhibit all cardinal features of inflammation, including increased circulating levels of inflammatory inducers, activated sensors, and inflammatory mediators targeting all tissues. Inflammation may contribute to the pathophysiology and clinical progression of these disorders. Of note, proinflammatory cytokines modulate mood behavior and cognition by reducing brain monoamine levels, activating neuroendocrine responses, promoting excitotoxicity (increased glutamate levels), and impairing brain plasticity. What are the sources of this chronic inflammation? Increasing evidence indicates that changes in neuroendocrine regulation, metabolism, diet/microbiota, and negative health behaviors are important triggers of inflammation. Finally, recent data indicate that early-life stress is associated with overt inflammation prior to the development of neuropsychiatric disorders.

show abstract

The effects of early life adversity on the immune system

Cited by 151 publications

References 164 publications

Old Friends, immunoregulation, and stress resilience

Old Friends, immunoregulation, and stress resilience

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

Inflammation in psychiatric disorders: what comes first?

Contact Info

Product

Resources

About