Social stress up-regulates inflammatory gene expression in the leukocyte transcriptome via β-adrenergic induction of myelopoiesis

Powell, Nicole D.; Sloan, Erica K.; Bailey, Michael T.; Arevalo, Jesusa M.G.; Miller, Gregory E.; Chen, Eric; Kobor, Michæl S.; Reader, Brenda F.; Sheridan, John F.; Cole, Steven W.

doi:10.1073/pnas.1310655110

Cited by 510 publications

(564 citation statements)

References 63 publications

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“…It also remains to be determined which neurobiological pathways mediate the effects of prosocial behavior. This is a particularly intriguing question in light of previous data showing that CTRA expression is biologically mediated in large part by threat-related systems (i.e., sympathetic nervous system/β-adrenergic signaling; Cole, 2014;Cole et al, 2015a;Powell et al, 2013). Defining the upstream neurobiological mediators in the CNS substrates of prosocial experience also remains an important topic for future research (Eisenberger and Cole, 2012).…”

Section: Psychobiological Mechanismsmentioning

confidence: 98%

“…This research has identified a conserved transcriptional response to adversity (CTRA) in circulating leukocytes that is characterized by up-regulation of pro-inflammatory genes and down-regulation of genes involved in innate antiviral responses and antibody production (Cole, 2014;Slavich and Cole, 2013). The CTRA gene expression profile is mediated by both per-cell alterations in gene transcription and increased production of specific subtypes of leukocytes (particularly myeloid lineage monocytes and dendritic cells; Cole et al, 2011;Cole, 2014;Powell et al, 2013;Slavich and Cole, 2013). These dynamics are mediated by activation of β-adrenergic signaling pathways in response to sympathetic nervous system activity and take place over the course of several hours to a few days (Cole, 2010(Cole, , 2014Cole et al, 2015a;Powell et al, 2013;Slavich and Cole, 2013).…”

Section: Human Social Genomicsmentioning

confidence: 99%

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Kindness in the blood: A randomized controlled trial of the gene regulatory impact of prosocial behavior

Nelson‐Coffey

Fritz

Lyubomirsky

et al. 2017

Psychoneuroendocrinology

112

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A B S T R A C TContext: Prosocial behavior is linked to longevity, but few studies have experimentally manipulated prosocial behavior to identify the causal mechanisms underlying this association. One possible mediating pathway involves changes in gene expression that may subsequently influence disease development or resistance. Design, setting, participants: In the current study, we examined changes in a leukocyte gene expression profile known as the Conserved Transcriptional Response to Adversity (CTRA) in 159 adults who were randomly assigned for 4 weeks to engage in prosocial behavior directed towards specific others, prosocial behavior directed towards the world in general, self-focused kindness, or a neutral control task. Results: Those randomized to prosocial behavior towards specific others demonstrated improvements (i.e., reductions) in leukocyte expression of CTRA indicator genes. No significant changes in CTRA gene expression were observed in the other 3 conditions. Conclusion: These findings suggest that prosocial behavior can causally impact leukocyte gene expression profiles in ways that might potentially help explain the previously observed health advantages associated with social ties.

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Section: Psychobiological Mechanismsmentioning

confidence: 98%

Section: Human Social Genomicsmentioning

confidence: 99%

Kindness in the blood: A randomized controlled trial of the gene regulatory impact of prosocial behavior

Nelson‐Coffey

Fritz

Lyubomirsky

et al. 2017

Psychoneuroendocrinology

112

View full text Add to dashboard Cite

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“…76 In addition, animal research in mice has identified upregulation of inflammatory gene expression in the presence of social stress. 77 …”

Section: The Pathophysiology Of Poverty Toxic Stressmentioning

confidence: 99%

Mediators and Adverse Effects of Child Poverty in the United States

Pascoe¹,

Wood²,

Duffee³

et al. 2016

Pediatrics

134

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The link between poverty and children's health is well recognized. Even temporary poverty may have an adverse effect on children's health, and data consistently support the observation that poverty in childhood continues to have a negative effect on health into adulthood. In addition to childhood morbidity being related to child poverty, epidemiologic studies have documented a mortality gradient for children aged 1 to 15 years (and adults), with poor children experiencing a higher mortality rate than children from higher-income families. The global great recession is only now very slowly abating for millions of America's children and their families. At this diffi cult time in the history of our nation's families and immediately after the 50th anniversary year of President Lyndon Johnson's War on Poverty, it is particularly germane for the American Academy of Pediatrics, which is "dedicated to the health of all children, " to publish a research-supported technical report that examines the mediators associated with the longrecognized adverse effects of child poverty on children and their families. This technical report draws on research from a number of disciplines, including physiology, sociology, psychology, economics, and epidemiology, to describe the present state of knowledge regarding poverty's negative impact on children's health and development. Children inherit not only their parents' genes but also the family ecology and its social milieu. Thus, parenting skills, housing, neighborhood, schools, and other factors (eg, medical care) all have complex relations to each other and infl uence how each child's genetic canvas is expressed. Accompanying this technical report is a policy statement that describes specifi c actions that pediatricians and other child advocates can take to attenuate the negative effects of the mediators identifi ed in this technical report and improve the well-being of our nation's children and their families.There is no keener revelation of a society's soul than the way in which it treats its children. Although medical care and access to medical care are important factors in the health of children as well as adults, a broader perspective of the social determinants of health throughout the life cycle is critically important if significant gains are to be realized in our efforts to improve the health of this nation's children. -Nelson Mandela TECHNICAL REPORTResearch that examines mediators of health as well as the effects of poverty and other circumstances in which people grow, live, work, and age in childhood and throughout the life course is accumulating rapidly, and findings are providing critical insights that can inform these efforts. 4 The environment in which a child develops is influenced by parents' health, the immediate and extended family, housing, and community. All these factors are related to a family's social, economic, and health status. 5 These multiple factors in both the social and the physical domains have dynamic influences that link them to the long-t...

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“…Epigenetic or other alterations in response to stress during "critical periods" of growth and development may modify brain function, and thus sensitize neural responsiveness to traumatic situations later in life. For instance, under stressful conditions, the persistently sensitized brain may elicit a heightened sympathetic nervous system response-the response associated with fight-or-flight-which has been shown to up-regulate sub-populations of immature monocytes, prompting increased leukocyte expression of proinflammatory genes (Powell et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Childhood and Later Life Stressors and Increased Inflammatory Gene Expression at Older ages

2016

The Gerontologist

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Adverse experiences in early life have the ability to "get under the skin" and affect future health. This study examined the relative influence of adversities during childhood and adulthood in accounting for individual differences in pro-inflammatory gene expression in late life. Using a pilot-sample from the Health and Retirement Study (N=114) aged from 51-95, OLS regression models were run to determine the association between a composite score from three proinflammatory gene expression levels (PTGS2, ILIB, and IL8) and 1) childhood trauma, 2) childhood SES, 3) childhood health, 4) adult traumas, and 5) low SES in adulthood. Our results showed that only childhood trauma was found to be associated with increased inflammatory transcription in late life. Furthermore, examination of interaction effects showed that childhood trauma exacerbated the influence of low SES in adulthood on elevated levels of inflammatory gene expression-signifying that having low SES in adulthood was most damaging for persons who had experienced traumatic events during their childhood. Overall our study suggests that traumas experienced during childhood may alter the stress response, leading to more sensitive reactivity throughout the lifespan. As a result, individuals who experienced greater adversity in early life may be at higher risk of late life health outcomes, particularly if adulthood adversity related to SES persists.

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Social stress up-regulates inflammatory gene expression in the leukocyte transcriptome via β-adrenergic induction of myelopoiesis

Cited by 510 publications

References 63 publications

Kindness in the blood: A randomized controlled trial of the gene regulatory impact of prosocial behavior

Kindness in the blood: A randomized controlled trial of the gene regulatory impact of prosocial behavior

Mediators and Adverse Effects of Child Poverty in the United States

Childhood and Later Life Stressors and Increased Inflammatory Gene Expression at Older ages

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