Acute inflammation and negative mood: Mediation by cytokine activation

Wright, Caroline; Strike, Philip C.; Brydon, Lena; Steptoe, Andrew

doi:10.1016/j.bbi.2004.10.003

Cited by 251 publications

(195 citation statements)

References 29 publications

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“…[212][213][214][215][216] In addition, inflammatory diseases are typically associated with depressed mood. 217,218 Administration of proinflammatory cytokines (e.g. in cancer or hepatitis C therapy) has been found to induce depressive symptoms.…”

Section: Stressmentioning

confidence: 99%

“…Several studies in healthy volunteers have suggested that increased concentrations of IL-6, but also of TNF-a and IL-1 receptor antagonist (IL-1Ra) may cause depressed mood. [218][219][220] The increase of several proinflammatory cytokines appear to correlate with the severity of depressive symptom. 214,215,217,218,221 The 'cytokine theory of depression' implies that proinflammatory cytokines, acting as neuromodulators, represent the key factor in the (central) mediation of the behavioral, neuroendocrine and neurochemical features of depressive disorders.…”

Section: Stressmentioning

confidence: 99%

“…[218][219][220] The increase of several proinflammatory cytokines appear to correlate with the severity of depressive symptom. 214,215,217,218,221 The 'cytokine theory of depression' implies that proinflammatory cytokines, acting as neuromodulators, represent the key factor in the (central) mediation of the behavioral, neuroendocrine and neurochemical features of depressive disorders. 211,222 Proinflammatory cytokines increase 5-HT turnover, which may lead to depletion of 5-HT in combination with several other mechanisms that lower 5-HT.…”

Section: Stressmentioning

confidence: 99%

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Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system. Several factors that may disrupt the 5-HTergic system and hence contribute to SV are discussed, including genetic factors, female gender, personality characteristics, several types of stress and drug use. It is explained that SV can be demonstrated by means of manipulations of the 5-HTergic system, such as 5-HT challenges or acute tryptophan depletion (ATD). Results of 5-HT challenge studies and ATD studies are discussed in terms of their implications for the concept of SV. A model is proposed in which a combination of various factors that may compromise 5-HT functioning in one person can result in depression or other 5-HT-related pathology. By manipulating 5-HT levels, in particular with ATD, vulnerable subjects may be identified before pathology initiates, providing the opportunity to take preventive action. Although it is not likely that this model applies to all cases of depression, or is able to identify all vulnerable subjects, the strength of the model is that it may enable identification of vulnerable subjects before the 5-HT related pathology occurs. Molecular Psychiatry ( Keywords: serotonin; mood disorders; stress; genetics; sex; tryptophan Involvement of serotonin in depressionMood disorders are one of the most prevalent forms of mental illness. 1 According to the DSM-IV, the lifetime risk for major depressive disorder is between 10 and 25% for women and between 5 and 12% for men. 2 Depression has been studied intensively during the last few decades, but the psychological and neurobiological determinants of depression have not yet been precisely defined. Although several factors are known to contribute to the etiology of depression, it is not clear how these factors cause depression, and why some subjects become depressed while others remain unaffected. In terms of biological factors in the etiology of depression, there are several hypotheses. These include neurotransmitter dysfunctions (serotonin, 5-HT; dopamine, DA; norepinephrine, NE); dysregulations in hypothalamic-pituitary-adrenal (HPA) axis activity; and immune system imbalance. The aim of this article is not to discuss all of these hypotheses in detail, but to evaluate the role that serotonin may play within these hypothesized mechanisms.It is widely accepted that diminished serotonergic (5-HTergic) function is involved in the onset and course of depression. 3,4 The 5-HTergic system is a large and complex system. Although nearly all cell bodies of 5-HTergic neurons are located in the raphe nuclei in the brain stem, the axons of these neurons innervate almost the entire brain. The actions of 5-HT are mediated by 16 types and subtypes of receptors. 5 As the 5-HTergic system is assumed to be a modulatory system, the exact func...

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Section: Stressmentioning

confidence: 99%

Section: Stressmentioning

confidence: 99%

Section: Stressmentioning

confidence: 99%

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Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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“…Such withdrawal is achieved through decreased serotonic and dopaminergic activity, and HPA 310 dysregulation [68,69]. The stress reaction to sadness is similar in purpose, and refers to changes in the immune response, particularly to the heightened inflammatory responses [70,71], which are all associated with negative mood states.…”

Section: A Biological Systems Accountmentioning

confidence: 99%

An integrative review of the enjoyment of sadness associated with music

Eerola

Vuoskoski

Peltola

et al. 2018

Physics of Life Reviews

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Citation for published item:ierolD F nd uoskoskiD tF uF nd eltolD rFEF nd utkinenD F nd h¤ ferD uF @PHIUA 9en integrtive review of the enjoyment of sdness ssoited with musiF9D hysis of life reviewsF F Further information on publisher's website: httpsXGGdoiForgGIHFIHITGjFplrevFPHIUFIIFHIT Publisher's copyright statement:Additional information: Use policyThe full-text may be used and/or reproduced, and given to third parties in any format or medium, without prior permission or charge, for personal research or study, educational, or not-for-prot purposes provided that:• a full bibliographic reference is made to the original source • a link is made to the metadata record in DRO • the full-text is not changed in any way The full-text must not be sold in any format or medium without the formal permission of the copyright holders.Please consult the full DRO policy for further details. AbstractThe recent surge of interest towards the paradoxical pleasure produced by sad music has generated a handful of theories and an array of empirical explorations on the topic. However, none of these have attempted to weigh the existing evidence in a systematic fashion. The present work puts forward an integrative framework laid out over three levels of explanation -biological, psycho-social, and cultural -to compare and integrate the existing findings in a meaningful way. First, we review the evidence pertinent to experiences of pleasure associated with sad music from the fields of neuroscience, psychophysiology, and endocrinology. Then, the psychological and interpersonal mechanisms underlying the recognition and induction of sadness in the context of music are combined with putative explanations ranging from social surrogacy and nostalgia to feelings of being moved. Finally, we address the cultural aspects of the paradox -the extent to which it is embedded in the Western notion of music as an aesthetic, contemplative object -by synthesising findings from history, ethnography, and empirical studies. Furthermore, we complement these explanations by considering the particularly significant life meanings that sadness portrayed in art can evoke in some perceivers. Our central claim is that one cannot attribute the enjoyment of sadness fully to any one of these levels, but to a chain * Corresponding author Email address: tuomas.eerola@durham.ac.uk (Tuomas Eerola)Preprint submitted to Physics of Life Reviews November 10, 2017 of functionalities afforded by each level. Each explanatory level has several putative explanations and its own shift towards positive valence, but none of them deliver the full transformation from a highly negative experience to a fully enjoyable experience alone. The current evidence within this framework ranges from weak to non-existent at the biological level, moderate at the psychological level, and suggestive at the cultural level. We propose a series of focussed topics for future investigation that would allow to deconstruct the drivers and constraints of the processes leading to pleasurable music-related sad...

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“…In these studies, a peak inflammatory cytokine response was observed 6 hours following both inflammatory stimuli (Antoniades et al, 2011;MacIntyre et al, 2001;Paine et al, 2013b;Paulsen et al, 2005). The use of a low dose typhoid vaccination to induce a mild systemic inflammatory response is typically safe and approved by the US food and drug agency (Hingorani et al, 2000;Strike et al, 2004;Wright et al, 2005). The administration of a mild pathogen can stimulate the adaptive immune system to respond by mobilising white blood cells and increasing the production of inflammatory cytokines (Paine et al, 2013b).…”

Section: Introductionmentioning

confidence: 99%