Sex differences in post-traumatic stress disorder risk: autonomic control and inflammation

Fonkoue, Ida T.; Michopoulos, Vasiliki; Park, Jeanie

doi:10.1007/s10286-020-00729-7

Cited by 31 publications

(22 citation statements)

References 101 publications

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“…All COVID-19-related manuscripts are Open Access immediately upon publication. We also published a special issue on sex differences in cardiovascular autonomic control [ 1 , 3 , 4 , 8 , 9 , 11 ]. The reception of these series was exceptionally good.…”

mentioning

confidence: 99%

Three decades of Clinical Autonomic Research and beyond

Kaufmann

Jordan

2021

Clin Auton Res

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mentioning

confidence: 99%

Three decades of Clinical Autonomic Research and beyond

Kaufmann

Jordan

2021

Clin Auton Res

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“…160,173 Sex differences in the relationship between inflammation and human behavior are substantive enough that many researchers are now urging the field to explicitly evaluate sex as a biological variable in future research. 157,158,160,168,174 Data explicitly examining the role of sex in the relationship between inflammation, neurocircuitry, and the three RDoC components examined in this article (reward processing, motor processing, and threat reactivity) are currently sparse, but a few preliminary observations can be posited. First, sex differences may influence the relationship between reward processing and inflammation that are mediated by corticostriatal circuitry.…”

Section: Sex Differences In the Effects Of Inflammation On Behaviormentioning

confidence: 99%

Brick by Brick: Building a Transdiagnostic Understanding of Inflammation in Psychiatry

Thylur

Goldsmith

2022

Harv Rev Psychiatry

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Inflammatory phenomena are found in many psychiatric disorders-notably, depression, schizophrenia, and posttraumatic stress disorder. Inflammation has been linked to severity and treatment resistance, and may both contribute to, and result from, the pathophysiology of some psychiatric illnesses. Emerging research suggests that inflammation may contribute to symptom domains of reward, motor processing, and threat reactivity across different psychiatric diagnoses. Reward-processing deficits contribute to motivational impairments in depression and schizophrenia, and motorprocessing deficits contribute to psychomotor slowing in both depression and schizophrenia. A number of experimental models and clinical trials suggest that inflammation produces deficits in reward and motor processing through common pathways connecting the cortex and the striatum, which includes the nucleus accumbens, caudate nucleus, and putamen. The observed effects of inflammation on psychiatric disorders may cut across traditional conceptualizations of psychiatric diagnoses. Further study may lead to targeted immunomodulating treatments that address difficult-to-treat symptoms in a number of psychiatric disorders. In this review, we use a Research Domain Criteria framework to discuss proposed mechanisms for inflammation and its effects on the domains of reward processing, psychomotor slowing, and threat reactivity. We also discuss data that support contributing roles of metabolic dysregulation and sex differences on the behavioral outcomes of inflammation. Finally, we discuss ways that future studies can help disentangle this complex topic to yield fruitful results that will help advance the field of psychoneuroimmunology.

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“…Several reports link PTSD with increased inflammation and occurrence of inflammatory disorders (16)(17)(18)(19)(20)(21)(22)(23)(24)(25). In an early report by Gola et al, researchers found that peripheral blood mononuclear cells (PBMCs) from PTSD patients exhibited a more pre-activated phenotype, having higher levels of secreting inflammatory cytokines, such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a), and IL-1b when compared to control samples (26).…”

Section: Introductionmentioning

confidence: 99%

Dysregulated TP53 Among PTSD Patients Leads to Downregulation of miRNA let-7a and Promotes an Inflammatory Th17 Phenotype

et al. 2022

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Post-traumatic stress disorder (PTSD) is a psychiatric disorder and patients diagnosed with PTSD often express other comorbid health issues, particularly autoimmune and inflammatory disorders. Our previous reports investigating peripheral blood mononuclear cells (PBMCs) from PTSD patients showed that these patients exhibit an increased inflammatory T helper (Th) cell phenotype and widespread downregulation of microRNAs (miRNAs), key molecules involved in post-transcriptional gene regulation. A combination of analyzing prior datasets on gene and miRNA expression of PBMCs from PTSD and Control samples, as well as experiments using primary PBMCs collected from human PTSD and Controls blood, was used to evaluate TP53 expression, DNA methylation, and miRNA modulation on Th17 development. In the current report, we note several downregulated miRNAs were linked to tumor protein 53 (TP53), also known as p53. Expression data from PBMCs revealed that compared to Controls, PTSD patients exhibited decreased TP53 which correlated with an increased inflammatory Th17 phenotype. Decreased expression of TP53 in the PTSD population was shown to be associated with an increase in DNA methylation in the TP53 promotor region. Lastly, the most significantly downregulated TP53-associated miRNA, let-7a, was shown to negatively regulate Th17 T cells. Let-7a modulation in activated CD4+ T cells was shown to influence Th17 development and function, via alterations in IL-6 and IL-17 production, respectively. Collectively, these studies reveal that PTSD patients could be susceptible to inflammation by epigenetic dysregulation of TP53, which alters the miRNA profile to favor a proinflammatory Th17 phenotype.

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Sex differences in post-traumatic stress disorder risk: autonomic control and inflammation

Cited by 31 publications

References 101 publications

Three decades of Clinical Autonomic Research and beyond

Three decades of Clinical Autonomic Research and beyond

Brick by Brick: Building a Transdiagnostic Understanding of Inflammation in Psychiatry

Dysregulated TP53 Among PTSD Patients Leads to Downregulation of miRNA let-7a and Promotes an Inflammatory Th17 Phenotype

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