Consistent evidence indicates the association between inflammatory markers and suicidal behavior. The burden related to immunological differences have been widely documented in both major affective disorders and suicidal behavior. Importantly, abnormally elevated pro-inflammatory cytokines levels have been reported to correlate with suicidal behavior but whether and to what extent specific inflammatory cytokines abnormalities may contribute to our understanding of the complex pathophysiology of suicide is unknown. The present manuscript aimed to systematically review the current literature about the role of pro-inflammatory cytokines in suicidal behavior. Most studies showed a link between abnormally higher interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β1, vascular endothelial growth factor (VEGF), kynurenic acid (KYN), and lower IL-2, IL-4, and interferon (IFN)-γ levels in specific brain regions and suicidal behavior. Unfortunately, most studies are not able to exclude the exact contribution of major depressive disorder (MDD) as a mediator/moderator of the link between inflammatory cytokines abnormalities and suicidal behavior. The association between suicidal patients (both suicide attempters or those with suicidal ideation) and the altered immune system was documented by most studies, but this does not reflect the existence of a specific causal link. Additional studies are needed to clarify the immune pathways underlying suicidal behavior.

A Specific Inflammatory Profile Underlying Suicide Risk? Systematic Review of the Main Literature Findings / Serafini, Gianluca; Parisi, Valentina Maria; Aguglia, Andrea; Amerio, Andrea; Sampogna, Gaia; Fiorillo, Andrea; Pompili, Maurizio; Amore, Mario. - In: INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH. - ISSN 1660-4601. - 17:7(2020), p. 2393. [10.3390/ijerph17072393]

A Specific Inflammatory Profile Underlying Suicide Risk? Systematic Review of the Main Literature Findings

Pompili, Maurizio
Penultimo
;
2020

Abstract

Consistent evidence indicates the association between inflammatory markers and suicidal behavior. The burden related to immunological differences have been widely documented in both major affective disorders and suicidal behavior. Importantly, abnormally elevated pro-inflammatory cytokines levels have been reported to correlate with suicidal behavior but whether and to what extent specific inflammatory cytokines abnormalities may contribute to our understanding of the complex pathophysiology of suicide is unknown. The present manuscript aimed to systematically review the current literature about the role of pro-inflammatory cytokines in suicidal behavior. Most studies showed a link between abnormally higher interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β1, vascular endothelial growth factor (VEGF), kynurenic acid (KYN), and lower IL-2, IL-4, and interferon (IFN)-γ levels in specific brain regions and suicidal behavior. Unfortunately, most studies are not able to exclude the exact contribution of major depressive disorder (MDD) as a mediator/moderator of the link between inflammatory cytokines abnormalities and suicidal behavior. The association between suicidal patients (both suicide attempters or those with suicidal ideation) and the altered immune system was documented by most studies, but this does not reflect the existence of a specific causal link. Additional studies are needed to clarify the immune pathways underlying suicidal behavior.
2020
immune pathways; immunological differences; inflammatory cytokines; major depressive disorder; suicidal behavior.
01 Pubblicazione su rivista::01a Articolo in rivista
A Specific Inflammatory Profile Underlying Suicide Risk? Systematic Review of the Main Literature Findings / Serafini, Gianluca; Parisi, Valentina Maria; Aguglia, Andrea; Amerio, Andrea; Sampogna, Gaia; Fiorillo, Andrea; Pompili, Maurizio; Amore, Mario. - In: INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH. - ISSN 1660-4601. - 17:7(2020), p. 2393. [10.3390/ijerph17072393]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1520466
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