Psychiatric Symptoms in Survivors of Acute Respiratory Distress Syndrome. Effects of Age, Sex, and Immune Modulation

Spencer-Segal, Joanna L.; Hyzy, Robert C.; Iwashyna, Theodore J.; Standiford, Theodore J.

doi:10.1513/annalsats.201606-468oc

Cited by 26 publications

(23 citation statements)

References 44 publications

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“…This study speculated that the chronic inflammatory state associated with the traumatic brain injury results in elevated cytokine levels in the central nervous system and, in turn, microglial over-activation. In a clinical trial, patients with acute respiratory distress who were treated with GM-CSF had more severe PTSD symptoms than those treated with placebo ( 57 ). Since GM-CSF stimulates proliferation and differentiation of hematopoietic cells and can cross the blood–brain barrier, this study suggested the possibility of GM-CSF stimulating either brain microglia or production of inflammatory cytokines within the brain to result in more severe PTSD.…”

Section: Clinical Impacts Of Immune Imbalances In Ptsdmentioning

confidence: 99%

Posttraumatic Stress Disorder: An Immunological Disorder?

2017

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Patients with posttraumatic stress disorder (PTSD) exhibit an increased state of inflammation. Various animal models for PTSD have shown some of the same immune imbalances as have been shown in human subjects with PTSD, and some of these studies are discussed in this review. However, animal studies can only indirectly implicate immune involvement in PTSD in humans. This review of mainly studies with human subjects focuses on dissecting the immunological role in the pathogenesis of PTSD following initial trauma exposure. It addresses both the inflammatory state associated with PTSD and the immune imbalance between stimulatory and inhibitory immune mediators, as well as variables that can lead to discrepancies between analyses. The concept of immunological treatment approaches is proposed for PTSD, as new treatments are needed for this devastating disorder that is affecting unprecedented numbers of Veterans from the long-standing wars in the Middle East and which affects civilians following severe trauma.

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Section: Clinical Impacts Of Immune Imbalances In Ptsdmentioning

confidence: 99%

Posttraumatic Stress Disorder: An Immunological Disorder?

2017

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“…Alternatively, altered trafficking of activated peripheral immune cells in states of peripheral inflammation through the blood-CSF barrier has been suggested to contribute to triggering and perpetuation of depression and PTSD [2]. Intriguingly, administration of GM-CSF to patients suffering acute respiratory distress syndrome has recently been reported to associate with increased rates of PTSD symptoms at follow-up [23]. High peripheral G-CSF levels have been suggested to contribute to a proinflammatory state exacerbating the course of coronary heart disease, and reduc- ing the level of G-CSF during myocardial infarction has been shown to reduce damage to the heart muscle [24].…”

Section: Discussionmentioning

confidence: 99%

Long-Term Immune Alterations Accompanying Chronic Posttraumatic Stress Disorder following Exposure to Suicide Bomb Terror Incidents during Childhood

et al. 2017

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Background and Aim: Long-term immune alterations have been proposed to play a mechanistic role in posttraumatic stress disorder (PTSD) as well as in its associated increase in medical morbidity and mortality. Better characterization of altered immune function may help identify diagnostic and prognostic biomarkers and potentially targets for preventive intervention. Methods: As part of an ongoing study, we conducted a preliminary case-control comparison of resting immune inflammatory profiles between terror victims treated in childhood at the emergency department over the previous decade, who developed chronic PTSD upon long-term follow-up, and healthy controls. Results: Our preliminary results in a subsample of this ongoing study support and extend elevated resting levels of granulocyte colony-stimulating factor, interleukin-4, and regulated on activation, normal T cell expressed and secreted in childhood onset chronic PTSD. Conclusion: Chronic immune alterations may participate in inflammatory activation and signal to the CNS through the neurovascular unit, as well as modulate the neuroendocrine axis. Better characterization and understanding of these preliminary findings may point to diagnostic and prognostic biomarkers and potentially elucidate mechanistic involvement of immune activation in PTSD.

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“…While GM-CSF was also linked to depression and anxiety score elevation in ARDS patients, corticosteroids, which reduce the inflammatory response, had the opposite effect on these disorders [41].GM-CSF expression is stimulated by pro-inflammatory cytokines and inhibited by anti-inflammatory cytokines and also serves to both stimulate and regulate pro-inflammatory cytokines, thus suggesting a direct role in the activation of type I macrophages, which have been linked to GAD and associated depressive disorders [44].…”

Section: The Diaeventological Axismentioning

confidence: 99%

“…Macrophage polarity and activation are linked to neuropsychiatric conditions including GAD and MDD. A case in point is acute respiratory distress syndrome (ARDS) [41].…”

Section: The Diaeventological Axismentioning

confidence: 99%

“…ARDS pathology is characterized by injury to the capillary endothelia and subsequent damage to alveoli, severe arterial vasoconstriction, and pulmonary hypertension [42]. Subsequent to lung injury, ARDS patients are typically treated with granulocyte/macrophage colony stimulating factor (GM-CSF) as a component of their pharmacotherapy [41].…”

Section: The Diaeventological Axismentioning

confidence: 99%

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The Diaeventology of Anxiety Disorders

Guerra¹

2019

Anxiety Disorders - From Childhood to Adulthood

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Anxiety is a crippling neuropsychiatric condition that encompasses a complex endophenotypic network of genetic, immunological, epigenetic, and metabolic mechanisms, interacting with the environment. A new approach to complex biological systems, including mental states and their neurological correlates, is diaeventology, a paradigm that exposes the event ontologies of these biomolecular/cellular mechanisms. General anxiety disorder has been studied in subclinical and clinical research settings where evidence is obtained for a longitudinal patterning of chronic and episodic and often increasingly stressful life events that provide the etiology and development of the pathology. Early events that involve brain oxygen deprivation coupled with carbon dioxide abundance are linked to biochemical and epigenetic processes associated with anxiety instantiation. A verified analysis of the current evidence suggests a neuroimmune mechanism that aligns with stress pathophysiology and epigenetic re-tailoring of key genomic loci that inappropriately compensate and misdirect biological defense mechanisms toward central nervous system dysfunction presenting as anxiety disorders.

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Psychiatric Symptoms in Survivors of Acute Respiratory Distress Syndrome. Effects of Age, Sex, and Immune Modulation

Abstract: 6 months after ARDS, age, sex, illness severity, steroids, and GM-CSF treatment were associated with psychiatric symptom scores. These associations should be confirmed in a larger population. Clinical Trial registered with clinicaltrials.gov (NCT00201409).

Cited by 26 publications

References 44 publications

Posttraumatic Stress Disorder: An Immunological Disorder?

Posttraumatic Stress Disorder: An Immunological Disorder?

Long-Term Immune Alterations Accompanying Chronic Posttraumatic Stress Disorder following Exposure to Suicide Bomb Terror Incidents during Childhood

The Diaeventology of Anxiety Disorders

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