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Review
. 2023 Sep 4:22:928-945.
doi: 10.17179/excli2023-6391. eCollection 2023.

Metabolic and immune dysfunctions in post-traumatic stress disorder: what can we learn from animal models?

Oleh Lushchak  1   2 , Marco Orru  1 , Olha Strilbytska  1 , Vladyslav Berezovskyi  1 , Andriy Cherkas  2 , Kenneth B Storey  3 , Maria Bayliak  1
Affiliations
Review

Metabolic and immune dysfunctions in post-traumatic stress disorder: what can we learn from animal models?

Oleh Lushchak et al. EXCLI J. .

Abstract

Highly stressful experiences such as terrorist attacks, domestic and sexual violence may lead to persistent pathological symptoms such as those seen in posttraumatic stress disorder (PTSD). There is growing evidence of multiple metabolic and immune disorders underlying the etiology and maintenance of PTSD. However, changes in the functioning of various systems and organs associated with PTSD are not well understood. Studies of reliable animal models is one of the effective scientific tools that can be used to gain insight into the role of metabolism and immunity in the comorbidity associated with PTSD. Since much progress has been made using animal models to understand mechanisms of PTSD, we summarized metabolic and immune dysfunction in mice and humans to compare certain outcomes associated with PTSD. The systemic effects of PTSD include chronic activation of the sympathetic nervous system (psycho-emotional stress), that leads to impairment of the function of the immune system, increased release of stress hormones, and metabolic changes. We discuss PTSD as a multisystem disease with its neurological, immunological, and metabolic components.

Keywords: immunity; metabolism; post-traumatic stress disorder.

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Conflict of interest statement

There are no conflicts of interest to declare.

Figures

Table 1
Table 1. Description of rodent models of PTSD with metabolic and immune consequences
Figure 1
Figure 1. An overview of the neurological, metabolic and immunity imbalances in patients with PTSD. The hypothalamic-pituitary-adrenal (HPA) axis is the primary neuroendocrine pathway involved in stress response via release of secretions. Glucocorticoids appear to regulate various metabolic and immune processes. CRH, corticotropin-releasing hormone; ACTH, adrenocorticotrophic hormone; TNF, tumor necrosis factor; IL-6, interleukin-6; IL-1β, interleukin-1β; IL-2, interleukin-2.
Figure 2
Figure 2. Metabolic and immune responses in rodents and human. Physical or psychosocial stressors used to generate animal models of post-traumatic stress disorder that is associated with metabolic syndrome, obesity, diabetes and inflammation.
See this image and copyright information in PMC

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