Depression and sterile inflammation: Essential role of danger associated molecular patterns

Franklin, Tina; Xu, Chelsea Y.; Duman, Ronald S.

doi:10.1016/j.bbi.2017.10.025

Cited by 158 publications

(143 citation statements)

References 141 publications

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“…This stress‐related proinflammatory state represents ‘sterile inflammation’, that is, inflammation in the absence of pathogenic disease. Sterile inflammation can be triggered by the activation of pattern‐recognition receptors that detect endogenous ligands termed danger‐ (or damage‐)associated molecular patterns (DAMPs) . DAMPs are host‐derived, non‐microbial endogenous molecules that are increased in response to physical and psychological stress, and are considered to include a variety of different molecules, such as heat‐shock proteins, S100 proteins, high mobility group box 1, uric acids, and adenosine triphosphate .…”

Section: Mechanisms Underlying the Link Between Inflammation And Ptsdmentioning

confidence: 99%

“…Sterile inflammation can be triggered by the activation of pattern‐recognition receptors that detect endogenous ligands termed danger‐ (or damage‐)associated molecular patterns (DAMPs) . DAMPs are host‐derived, non‐microbial endogenous molecules that are increased in response to physical and psychological stress, and are considered to include a variety of different molecules, such as heat‐shock proteins, S100 proteins, high mobility group box 1, uric acids, and adenosine triphosphate . The binding of DAMPs to pattern‐recognition receptors can lead to sterile inflammation in both inflammasome‐independent and ‐dependent manners .…”

Section: Mechanisms Underlying the Link Between Inflammation And Ptsdmentioning

confidence: 99%

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Inflammation and post‐traumatic stress disorder

Hori

Kim

2019

Psychiatry Clin Neurosci

262

176

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While post‐traumatic stress disorder (PTSD) is currently diagnosed based solely on classic psychological and behavioral symptoms, a growing body of evidence has highlighted a link between this disorder and alterations in the immune and inflammatory systems. Epidemiological studies have demonstrated that PTSD is associated with significantly increased rates of physical comorbidities in which immune dysregulation is involved, such as metabolic syndrome, atherosclerotic cardiovascular disease, and autoimmune diseases. In line with this, a number of blood biomarker studies have reported that compared to healthy controls, individuals with PTSD exhibit significantly elevated levels of proinflammatory markers, such as interleukin‐1β, interleukin‐6, tumor necrosis factor‐α, and C‐reactive protein. Moreover, various lines of animal and human research have suggested that inflammation is not only associated with PTSD but also can play an important role in its pathogenesis and pathophysiology. In this review, we first summarize evidence suggestive of increased inflammation in PTSD. We then examine findings that suggest possible mechanisms of inflammation in this disorder in terms of two different but interrelated perspectives: putative causes of increased proinflammatory activities and potential consequences that inflammation generates. Given that there is currently a dearth of treatment options for PTSD, possibilities of new therapeutic approaches using pharmacological and non‐pharmacological treatments/interventions that have anti‐inflammatory effects are also discussed. Despite the increasing attention given to the inflammatory pathology of PTSD, there remains much to be elucidated, including more detailed mechanisms of inflammation, potential usefulness of inflammatory biomarkers as diagnostic and prognostic markers, and efficacy of novel treatment strategies targeting inflammation.

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Section: Mechanisms Underlying the Link Between Inflammation And Ptsdmentioning

confidence: 99%

Section: Mechanisms Underlying the Link Between Inflammation And Ptsdmentioning

confidence: 99%

Inflammation and post‐traumatic stress disorder

Hori

Kim

2019

Psychiatry Clin Neurosci

262

176

View full text Add to dashboard Cite

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“…; Fehily and Fitzgerald ; Mizuma and Yenari ; Neal and Richardson ; Franklin et al . ; Prata et al . ; Santos and Ferreira ; Joshi and Singh ; Thelin et al .…”

Section: Concluding Remarks and Perspectivesmentioning

confidence: 99%

“…The disorders considered in the present review are caused by different etiologic factors and display a variety of symptoms that could hardly be reconducted to a unifying pattern. However, regardless of the origin of these diseases, the involvement of processes which share aspects reasonably attributable to inflammation is detectable in their underlying pathogenic mechanisms (Giovannoni et al 2007;Wilcock and Griffin 2013;King et al 2014;Ochoa-Cortes et al 2016;Hamlett et al 2018;Stark et al 2016;Chitnis and Weiner 2017;Labzin et al 2018;Fehily and Fitzgerald 2017;Mizuma and Yenari 2017;Neal and Richardson 2017;Franklin et al 2017;Prata et al 2017;Santos and Ferreira 2017;Joshi and Singh 2017;Thelin et al 2017a;Majd et al 2017;Zhang et al 2017;Zolezzi and Inestrosa 2017). This consideration has also been the object of a recent valuable review (Skaper et al 2018).…”

Section: Concluding Remarks and Perspectivesmentioning

confidence: 99%

The S100B story: from biomarker to active factor in neural injury

Michetti

D’Ambrosi

Toesca

et al. 2018

Journal of Neurochemistry

273

238

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S100B is a Ca -binding protein mainly concentrated in astrocytes. Its levels in biological fluids (cerebrospinal fluid, peripheral and cord blood, urine, saliva, amniotic fluid) are recognized as a reliable biomarker of active neural distress. Although the wide spectrum of diseases in which the protein is involved (acute brain injury, neurodegenerative diseases, congenital/perinatal disorders, psychiatric disorders) reduces its specificity, its levels remain an important aid in monitoring the trend of the disorder. Mounting evidence now points to S100B as a Damage-Associated Molecular Pattern molecule which, when released at high concentration, through its Receptor for Advanced Glycation Endproducts, triggers tissue reaction to damage in a series of different neural disorders. This review addresses this novel scenario, presenting data indicating that S100B levels and/or distribution in the nervous tissue of patients and/or experimental models of different neural disorders, for which the protein is used as a biomarker, are directly related to the progress of the disease: acute brain injury (ischemic/hemorrhagic stroke, traumatic injury), neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis), congenital/perinatal disorders (Down syndrome, spinocerebellar ataxia-1), psychiatric disorders (schizophrenia, mood disorders), inflammatory bowel disease. In many cases, over-expression/administration of the protein induces worsening of the disease, whereas its deletion/inactivation produces amelioration. This review points out that the pivotal role of the protein resulting from these data, opens the perspective that S100B may be regarded as a therapeutic target for these different diseases, which appear to share some common features reasonably attributable to neuroinflammation, regardless their origin.

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“…For instance, the prevalence of anxiety and depressive disorders increases during adolescence, with women being diagnosed two to three times more than men. 5,[20][21][22][23] Research regarding the biological basis of sex differences in neural disorders has largely focused on hormones, 21,[24][25][26] inflammatory signaling 1,27,28 and neurotransmitters. 29 Here, we focus on possible structural maturation of the brain that may give rise to sex differences and later life susceptibility to neural disorders either independently or in concert with these factors.…”

mentioning

confidence: 99%

Adolescent maturation of the prefrontal cortex: Role of stress and sex in shaping adult risk for compromise

Shaw

Dupree

Neigh

2019

Genes Brain and Behavior

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Adolescence is a highly dynamic period of development, which includes the final organizational phases of neural maturation within the prefrontal cortex (PFC). The organizational events of neural pruning and myelination occur in a sex‐specific manner, potentially giving rise to the disparities in mood disorders in adulthood. Because of the extended developmental time period of the PFC, environmental insults, including psychosocial stressors, may play a major role in steering the maturation of this region. In this review, the literature surrounding the sex specific alterations that occur in the PFC in rodent models following adolescent stress will be discussed. This will be complimented by a brief review on the state of human research in PFC sex differences in the development of white matter and cytoarchitecture across the lifespan. Taken together, the impact of developmental psychosocial stress on the circuitry of the PFC and resulting adult phenotypes will be summarized with a focus on the importance of considering sex differences in order to build a better understanding of developmental influences on adult disorders.

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Depression and sterile inflammation: Essential role of danger associated molecular patterns

Cited by 158 publications

References 141 publications

Inflammation and post‐traumatic stress disorder

Inflammation and post‐traumatic stress disorder

The S100B story: from biomarker to active factor in neural injury

Adolescent maturation of the prefrontal cortex: Role of stress and sex in shaping adult risk for compromise

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