Inflammation in Post-Traumatic Stress Disorder (PTSD): A Review of Potential Correlates of PTSD with a Neurological Perspective

Kim, Tammy D.; Lee, Suji; Yoon, Sujung

doi:10.3390/antiox9020107

Cited by 95 publications

(65 citation statements)

References 111 publications

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“…In finding that peripheral inflammation in RSDS was most tightly- linked with the EZM—a test of anxiety-like behavior—it is worth noting the DSM-IV originally characterized PTSD under the umbrella of anxiety disorders ( American Psychiatric Association, 2000 ). There is a breadth of clinical literature demonstrating differences in peripheral inflammation in patients with PTSD as well as other anxiety disorders ( O’Donovan, 2015 ; Neigh and Ali, 2016 ; Boscarino, 2004 ; Kim et al, 2020 ; Renna et al, 2018 ). Importantly, many of the cytokines we found to be differentially elevated in control versus RSDS have also been shown to be elevated in human plasma from patients with PTSD, such as IL-2, IL-6, IL-17, and TNFα (summarized well by Wang et al ) ( Wang et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Peripheral inflammation is strongly linked to elevated zero maze behavior in repeated social defeat stress

Elkhatib

Moshfegh

Watson

et al. 2020

Brain, Behavior, and Immunity

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Post-traumatic stress disorder (PTSD) is a psychiatric illness that results in an increased risk for a variety of inflammatory diseases. The exact etiology of this increased risk is unknown, and thus several animal models have been developed to investigate the neuroimmune interactions of PTSD. Repeated social defeat stress (RSDS) is an established preclinical model of psychological trauma that recapitulates certain behavioral and inflammatory aspects of human PTSD. Furthermore, RSDS has been utilized to subgroup animals into susceptible and resilient populations based on one specific behavioral phenotype ( i.e. , social interaction). Herein, we conducted an extensive investigation of circulating inflammatory proteins after RSDS and found significant elevations in various cytokines and chemokines after exposure to RSDS. When categorizing animals into either susceptible or resilient populations based on social interaction, we found no inflammatory or other behavioral differences between these subgroups. Furthermore, correlative analyses found no significant correlation between social interaction parameters and inflammation. In contrast, parameters from the elevated zero maze (EZM) demonstrated significant associations and clustering to five circulating cytokines. When animals were subdivided into susceptible and resilient populations solely based upon combined EZM performance, significant inflammatory differences were evident between these groups. Strikingly, these circulating inflammatory proteins displayed a stronger predictive ability of EZM performance compared to social interaction test performance. These findings provide new insights into inflammatory markers associated with RSDS, and the utility of EZM to effectively group RSDS-exposed mice into populations with differential levels of peripheral inflammation.

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Section: Discussionmentioning

confidence: 99%

Peripheral inflammation is strongly linked to elevated zero maze behavior in repeated social defeat stress

Elkhatib

Moshfegh

Watson

et al. 2020

Brain, Behavior, and Immunity

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“…Within the preclinical literature, opioids also have been shown to increase the production of corticotropin-releasing factor mRNA [9], and plasma corticosterone levels in rats [10]. The elevated cortisol or corticotropin-releasing factor response associated with opioid use and withdrawal has prominent immune consequences, as it is related to altered cytokine expression in both human and animal models [11][12][13] and observed across multiple anxiety disorders, such as PTSD [14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Hippocampal TNF-α Signaling Mediates Heroin Withdrawal-Enhanced Fear Learning and Withdrawal-Induced Weight Loss

Parekh

Paniccia²,

Adams³

et al. 2021

Mol Neurobiol

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There is significant comorbidity of opioid use disorder (OUD) and post-traumatic stress disorder (PTSD) in clinical populations. However, the neurobiological mechanisms underlying the relationship between chronic opioid use and withdrawal and development of PTSD are poorly understood. Our previous work identified that chronic escalating heroin administration and withdrawal can produce enhanced fear learning, an animal model of hyperarousal, and is associated with an increase in dorsal hippocampal (DH) interleukin-1β (IL-1β). However, other cytokines, such as TNF-α, work synergistically with IL-1β and may have a role in the development of enhanced fear learning. Based on both translational rodent and clinical studies, TNF-α has been implicated in hyperarousal states of PTSD, and has an established role in hippocampal-dependent learning and memory. The first set of experiments tested the hypothesis that chronic heroin administration followed by withdrawal is capable of inducing alterations in DH TNF-α expression. The second set of experiments examined whether DH TNF-α expression is functionally relevant to the development of enhanced fear learning. We identified an increase of TNF-α immunoreactivity and positive cells at 0, 24, and 48 h into withdrawal in the dentate gyrus DH subregion. Interestingly, intra-DH infusions of etanercept (TNF-α inhibitor) 0, 24, and 48 h into heroin withdrawal prevented the development of enhanced fear learning and mitigated withdrawal-induced weight loss. Overall, these findings provide insight into the role of TNF-α in opioid withdrawal and the development of anxiety disorders such as PTSD.

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“…Fear of being infected, or dying, and uncertainty of the future all contribute to the psychological distress lived by the population ( Li et al, 2020b ; Mazza et al, 2020 ; Satici et al, 2020 ). Social isolation resulting from social distancing and quarantine, changes in lifestyle including sleep, economic recession, financial loss, as well as boredom, misinformation, and overexposure to media coverage of the pandemic can further contribute to this burden ( Brooks et al, 2020 ; Garfin et al, 2020 ; Kim et al, 2020 ; Thakur and Jain, 2020 ). These circumstances along with several others, such as student status, poor self-rated health, higher perceived stress load, worry about family, friends, and other acquaintances suspected of COVID-19, together with less family support, were all associated with an increased risk of developing depressive or anxious symptoms during the pandemic ( Vindegaard and Benros, 2020 ).…”

Section: The Cns Is Affected By the Psychosocial Stress Imposed By Thmentioning

confidence: 99%

Microglia Fighting for Neurological and Mental Health: On the Central Nervous System Frontline of COVID-19 Pandemic

Andrade

Šimončičová

Carrier

et al. 2021

Front. Cell. Neurosci.

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Coronavirus disease 2019 (COVID-19) is marked by cardio-respiratory alterations, with increasing reports also indicating neurological and psychiatric symptoms in infected individuals. During COVID-19 pathology, the central nervous system (CNS) is possibly affected by direct severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) invasion, exaggerated systemic inflammatory responses, or hypoxia. Psychosocial stress imposed by the pandemic further affects the CNS of COVID-19 patients, but also the non-infected population, potentially contributing to the emergence or exacerbation of various neurological or mental health disorders. Microglia are central players of the CNS homeostasis maintenance and inflammatory response that exert their crucial functions in coordination with other CNS cells. During homeostatic challenges to the brain parenchyma, microglia modify their density, morphology, and molecular signature, resulting in the adjustment of their functions. In this review, we discuss how microglia may be involved in the neuroprotective and neurotoxic responses against CNS insults deriving from COVID-19. We examine how these responses may explain, at least partially, the neurological and psychiatric manifestations reported in COVID-19 patients and the general population. Furthermore, we consider how microglia might contribute to increased CNS vulnerability in certain groups, such as aged individuals and people with pre-existing conditions.

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Inflammation in Post-Traumatic Stress Disorder (PTSD): A Review of Potential Correlates of PTSD with a Neurological Perspective

Cited by 95 publications

References 111 publications

Peripheral inflammation is strongly linked to elevated zero maze behavior in repeated social defeat stress

Peripheral inflammation is strongly linked to elevated zero maze behavior in repeated social defeat stress

Hippocampal TNF-α Signaling Mediates Heroin Withdrawal-Enhanced Fear Learning and Withdrawal-Induced Weight Loss

Microglia Fighting for Neurological and Mental Health: On the Central Nervous System Frontline of COVID-19 Pandemic

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