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  1. Article ; Online: Psychosocial predictors of the innate immune response to influenza vaccination.

    Kuhlman, Kate Ryan / Radin, Arielle / Cole, Steve W / Bower, Julienne E

    Psychoneuroendocrinology

    2024  Volume 163, Page(s) 106989

    Abstract: Experimental activation of the innate immune system has contributed significantly to both our understanding of how psychological factors influence immune function as well as how immune activity influences the brain and behavior. The annual influenza ... ...

    Abstract Experimental activation of the innate immune system has contributed significantly to both our understanding of how psychological factors influence immune function as well as how immune activity influences the brain and behavior. The annual influenza vaccine can be used to interrogate the effects of mild immune stimulation on day-to-day changes in psychological processes in human subjects that range across the lifespan and in both clinical and non-clinical populations. Yet, the immune response to the influenza vaccine in the days immediately following its administration are not well characterized. The present study describes changes in inflammatory and antiviral gene expression within circulating immune cells, plasma cytokines, and C-reactive protein (CRP) following receipt of the flu vaccine, and further reports the association between several common behavioral health factors and the acute immune response. Participants were 65 adults (mean age 18.81 ± 1.03 years; 66.2% female) who provided a blood sample immediately before and then 24 h after receiving the vaccine. A subsample also provided additional blood samples at 48 and 72 h. Plasma was assayed for CRP, IL-6, IL-10, IL-8, TNF-α, and IFN-γ, and peripheral blood mononuclear cell RNA was sequenced for evidence of change in expression of an a priori set of type 1 interferon (IFN) and inflammatory response genes (INFLAM). Plasma cytokines, CRP, and IFN response genes increased 24 h after vaccination, all ps < .001. The increase in IFN gene expression correlated with the observed increase in plasma cytokines and CRP, p < .0001. The immune response to influenza vaccination at 24-hours was moderated by anxiety symptoms, BMI, being female, sleep, and history of influenza vaccination. These factors and their associations with common immune challenges may be useful in studies interrogating the origins of immune dysregulation. The annual influenza vaccine is an accessible and reliable exogenous activator of both circulating and transcriptional markers of innate immune reactivity, with sensitivity to behavioral health factors relevant for psychoneuroimmunology research.
    MeSH term(s) Adult ; Humans ; Female ; Adolescent ; Young Adult ; Male ; Influenza Vaccines ; Influenza, Human/prevention & control ; Leukocytes, Mononuclear/metabolism ; Cytokines ; Immunity, Innate ; Vaccination ; Antibodies, Viral
    Chemical Substances Influenza Vaccines ; Cytokines ; Antibodies, Viral
    Language English
    Publishing date 2024-02-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 197636-9
    ISSN 1873-3360 ; 0306-4530
    ISSN (online) 1873-3360
    ISSN 0306-4530
    DOI 10.1016/j.psyneuen.2024.106989
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Loneliness, epigenetic age acceleration, and chronic health conditions.

    Freilich, Colin D / Markon, Kristian E / Cole, Steve W / Krueger, Robert F

    Psychology and aging

    2024  

    Abstract: Having associations with a range of adverse physical health outcomes including mortality, loneliness is increasingly recognized as a pressing public health concern, but the mechanisms studied to date do not yet explain all loneliness-related health risk. ...

    Abstract Having associations with a range of adverse physical health outcomes including mortality, loneliness is increasingly recognized as a pressing public health concern, but the mechanisms studied to date do not yet explain all loneliness-related health risk. We sought to evaluate whether epigenetic influences on DNA methylation could help explain the relationship between loneliness and health. To do so, we first estimated associations between loneliness and epigenetic age acceleration (EAA) in a subsample of participants in the study of midlife in the United States (
    Language English
    Publishing date 2024-04-18
    Publishing country United States
    Document type Journal Article
    ZDB-ID 635596-1
    ISSN 1939-1498 ; 0882-7974
    ISSN (online) 1939-1498
    ISSN 0882-7974
    DOI 10.1037/pag0000822
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Parasympathetic neural activity and the reciprocal regulation of innate antiviral and inflammatory genes in the human immune system.

    Sloan, Richard P / Cole, Steve W

    Brain, behavior, and immunity

    2021  Volume 98, Page(s) 251–256

    Abstract: The vagus nerve mediates parasympathetic nervous system control of peripheral physiological processes including cardiovascular activity and immune response. In mice, tonic vagal activation down-regulates inflammation via nicotinic acetylcholine receptor- ... ...

    Abstract The vagus nerve mediates parasympathetic nervous system control of peripheral physiological processes including cardiovascular activity and immune response. In mice, tonic vagal activation down-regulates inflammation via nicotinic acetylcholine receptor-mediated inhibition of the pro-inflammatory transcription factor NF-κB in monocyte/macrophages. Because Type I interferon and pro-inflammatory genes are regulated reciprocally at the level of transcription factor activation and cell differentiation, we hypothesized that vagal activity would up-regulate Type I interferon response genes concurrently with inflammatory downregulation in human immune cells. We mapped empirical individual differences in the circulating leukocyte transcriptome and vagal activity indexed by high frequency (0.15-0.40 Hz) heart rate variability (HF-HRV) in 380 participants in the Midlife in the US study. Here we show that promoter-based bioinformatics analyses linked greater HF-HRV to reduced NF-κB activity and increased activity of IRF transcription factors involved in Type I interferon response (independent of β-antagonists, BMI, smoking, heavy alcohol consumption, and demographic factors). Transcript origin analyses implicated myeloid lineage immune cells as targets, representing per-cell alterations in gene transcription as HF-HRV was not associated with differential prevalence of leukocyte subsets. These findings support the concept of parasympathetic inhibition of pro-inflammatory gene expression in humans and up-regulation of Type I interferons that could augment host defense against viral infections.
    MeSH term(s) Animals ; Antiviral Agents ; Humans ; Interferon Regulatory Factors ; Leukocytes/metabolism ; Mice ; NF-kappa B/metabolism ; Parasympathetic Nervous System
    Chemical Substances Antiviral Agents ; Interferon Regulatory Factors ; NF-kappa B
    Language English
    Publishing date 2021-08-13
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 639219-2
    ISSN 1090-2139 ; 0889-1591
    ISSN (online) 1090-2139
    ISSN 0889-1591
    DOI 10.1016/j.bbi.2021.08.217
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Childhood Maltreatment and Immune Cell Gene Regulation during Adolescence: Transcriptomics Highlight Non-Classical Monocytes.

    Kuhlman, Kate R / Cole, Steve W / Tan, Ece N / Swanson, James A / Rao, Uma

    Biomolecules

    2024  Volume 14, Issue 2

    Abstract: Childhood maltreatment has been repeatedly linked to a higher incidence of health conditions with an underlying proinflammatory component, such as asthma, chronic obstructive pulmonary disease, stroke, and cardiovascular disease. Childhood maltreatment ... ...

    Abstract Childhood maltreatment has been repeatedly linked to a higher incidence of health conditions with an underlying proinflammatory component, such as asthma, chronic obstructive pulmonary disease, stroke, and cardiovascular disease. Childhood maltreatment has also been linked to elevated systemic inflammation prior to the onset of disease. However, childhood maltreatment is highly comorbid with other risk factors which have also been linked to inflammation, namely major depression. The present analysis addresses this issue by assessing the association of maltreatment with genome-wide transcriptional profiling of immune cells collected from four orthogonal groups of adolescents (aged 13-17): maltreated and not maltreated in childhood, with and without major depressive disorder. Maltreatment and psychiatric history were determined using semi-structured clinical interviews and cross-validated using self-report questionnaires. Dried whole blood spots were collected from each participant (
    MeSH term(s) Humans ; Adolescent ; Child ; Depressive Disorder, Major/genetics ; Monocytes ; Inflammation ; Gene Expression Profiling ; Child Abuse/psychology
    Language English
    Publishing date 2024-02-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom14020220
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Smartphone mindfulness meditation training reduces Pro-inflammatory gene expression in stressed adults: A randomized controlled trial.

    Dutcher, Janine M / Cole, Steve W / Williams, Adrian C / Creswell, J David

    Brain, behavior, and immunity

    2022  Volume 103, Page(s) 171–177

    Abstract: Mindfulness meditation training has been shown to be an effective stress reduction strategy, but less is known about its immunoregulatory impact. In a randomized controlled trial of stressed customer service workers, the present study tested whether a 30- ...

    Abstract Mindfulness meditation training has been shown to be an effective stress reduction strategy, but less is known about its immunoregulatory impact. In a randomized controlled trial of stressed customer service workers, the present study tested whether a 30-day smartphone-based mindfulness meditation training program (compared to a problem-solving control program) would affect pro-inflammatory gene expression. Both interventions led to reductions in stress levels, but there was no difference in stress reduction between conditions. Consistent with predictions, mindfulness training reduced activity of the pro-inflammatory NF-κB transcription control pathway compared to the active control. These results suggest that mindfulness training may be a particularly effective method for improving immune cell gene expression in stressful work environments.
    MeSH term(s) Adult ; Gene Expression ; Humans ; Meditation/methods ; Mindfulness/methods ; Smartphone ; Stress, Psychological/genetics ; Stress, Psychological/therapy
    Language English
    Publishing date 2022-04-12
    Publishing country Netherlands
    Document type Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 639219-2
    ISSN 1090-2139 ; 0889-1591
    ISSN (online) 1090-2139
    ISSN 0889-1591
    DOI 10.1016/j.bbi.2022.04.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The role of inflammation in acute psychosocial stress-induced modulation of reward processing in healthy female adults.

    Boyle, Chloe C / Cole, Steve W / Irwin, Michael R / Eisenberger, Naomi I / Bower, Julienne E

    Brain, behavior, & immunity - health

    2023  Volume 28, Page(s) 100588

    Abstract: Background: Anhedonia, or loss of interest and pleasure, is a pernicious symptom of depression that involves deficits in reward processing. Stress-induced inflammation is a plausible biopsychosocial mechanism of reward deficits, but little is known ... ...

    Abstract Background: Anhedonia, or loss of interest and pleasure, is a pernicious symptom of depression that involves deficits in reward processing. Stress-induced inflammation is a plausible biopsychosocial mechanism of reward deficits, but little is known whether stress-induced inflammation alters reward behavior. The present study (a secondary analysis of a completed randomized controlled trial) tested whether acute stress activated a key pro-inflammatory transcription control pathway, NF-κB, and whether this activation was associated with acute stress-induced modulation of reward processing.
    Methods: Healthy female adults (age 18-25) were randomized to undergo an acute psychosocial stressor (Trier Social Stress Test;
    Results: Relative to the control condition, stress increased bioinformatic measures of NF-κB transcription factor activity (
    Conclusions: Acute stress increases inflammatory signaling, and this effect is associated with increased reward processing. This demonstrates the reward system to be highly sensitive to inflammatory signaling, including the relatively mild alterations that occur following a single episode of acute psychosocial stress.
    Language English
    Publishing date 2023-01-09
    Publishing country United States
    Document type Journal Article
    ISSN 2666-3546
    ISSN (online) 2666-3546
    DOI 10.1016/j.bbih.2023.100588
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  7. Article ; Online: Type I interferons, inflammation, and fatigue in a longitudinal RNA study of women with breast cancer.

    Bower, Julienne E / Ganz, Patricia A / Irwin, Michael R / Crespi, Catherine M / Petersen, Laura / Asher, Arash / Hurvitz, Sara A / Cole, Steve W

    Brain, behavior, and immunity

    2024  Volume 118, Page(s) 312–317

    Abstract: Background: Fatigue is a common side effect of cancer and its treatment and is thought to be driven in part by activation of the proinflammatory cytokine network. However, the cellular and molecular underpinnings of cancer-related fatigue (CRF) have not ...

    Abstract Background: Fatigue is a common side effect of cancer and its treatment and is thought to be driven in part by activation of the proinflammatory cytokine network. However, the cellular and molecular underpinnings of cancer-related fatigue (CRF) have not been determined, nor have immune pathways beyond inflammation been carefully investigated. The goal of this study was to examine the association between CRF and activation of canonical proinflammatory gene regulation pathways and Type I interferon (IFN) signaling pathways in breast cancer patients during and after treatment.
    Methods: Women diagnosed with early-stage breast cancer (n = 181) completed assessments before and after treatment with radiation and/or chemotherapy and at 6, 12, and 18-month post-treatment follow-ups. Assessments included self-reported fatigue (Multidimensional Fatigue Symptom Inventory - Short Form) and expression of pre-specified sets of Type I IFN and pro-inflammatory immune response genes determined from mRNA sequencing of PBMCs. Mixed effect linear models examined changes in fatigue and immune gene expression over time and tested the hypothesis that fatigue would be associated with increased expression of Type I IFN and inflammatory response genes.
    Results: There were significant changes in fatigue and immune gene expression across the assessment period; all measures increased from pre- to post-treatment but showed diverging patterns over the follow-up, with declines in fatigue and persistent elevations in Type I IFN and proinflammatory gene expression. In mixed effect linear models, expression of Type I IFN response genes was elevated in association with fatigue across the assessment period, from pre-treatment to 18-month follow-up. In contrast, pro-inflammatory gene expression was associated with fatigue only at 6, 12, and 18-month follow-ups. Analyses controlling for changes in leukocyte subsets continued to show a significant association between fatigue and Type I IFN gene expression but reduced the time-dependent association with pro-inflammatory gene expression to non-significant.
    Conclusions: Results revealed unexpected complexity in the immune underpinnings of CRF and identify a novel role for IFN signaling as a robust contributor to this symptom before, during, and after treatment. Pro-inflammatory gene expression emerged as a predictor of fatigue later in the cancer trajectory, and that effect was primarily accounted for by a concurrent increase in monocyte prevalence.
    MeSH term(s) Humans ; Female ; Breast Neoplasms/complications ; Interferon Type I ; RNA ; Fatigue/genetics ; Inflammation/complications
    Chemical Substances Interferon Type I ; RNA (63231-63-0)
    Language English
    Publishing date 2024-02-05
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 639219-2
    ISSN 1090-2139 ; 0889-1591
    ISSN (online) 1090-2139
    ISSN 0889-1591
    DOI 10.1016/j.bbi.2024.02.003
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  8. Article ; Online: Psychoneuroimmunology in multiple myeloma and autologous hematopoietic stem cell transplant: Opportunities for research among patients and caregivers.

    Christian, Lisa M / Kiecolt-Glaser, Janice K / Cole, Steve W / Burd, Christin E / Madison, Annelise A / Wilson, Stephanie J / Rosko, Ashley E

    Brain, behavior, and immunity

    2024  Volume 119, Page(s) 507–519

    Abstract: Multiple myeloma (MM) is an incurable cancer and is the leading indication for autologous hematopoietic stem cell transplantation (HSCT). To be eligible for HSCT, a patient must have a caregiver, as caregivers play a central role in HSCT preparation and ... ...

    Abstract Multiple myeloma (MM) is an incurable cancer and is the leading indication for autologous hematopoietic stem cell transplantation (HSCT). To be eligible for HSCT, a patient must have a caregiver, as caregivers play a central role in HSCT preparation and recovery. MM patients remain on treatment indefinitely, and thus patients and their caregivers face long-term challenges including the intensity of HSCT and perpetual therapy after transplant. Importantly, both patients and their caregivers show heightened depressive and anxiety symptoms, with dyadic correspondence evidenced and caregivers' distress often exceeding that of patients. An extensive psychoneuroimmunology (PNI) literature links distress with health via immune and neuroendocrine dysregulation as well as biological aging. However, data on PNI in the context of multiple myeloma - in patients or caregivers - are remarkably limited. Distress in MM patients has been associated with poorer outcomes including higher inflammation, greater one year post-HSCT hospital readmissions, and worse overall survival. Further, anxiety and depression are linked to biological aging and may contribute to the poor long-term health of both patients and caregivers. Because MM generally affects older adults, individual differences in biological aging may represent an important modifier of MM biology and HSCT treatment outcomes. There are a number of clinical scenarios in which biologically younger people could be prescribed more intensive therapies, with potential for greater benefit, by using a personalized cancer therapy approach based on the quantification of physiologic reserve. Further, despite considerable psychological demands, the effects of distress on health among MM caregivers is largely unexamined. Within this context, the current critical review highlights gaps in knowledge at the intersection of HSCT, inflammation, and biological aging in the context of MM. Research in this area hold promise for opportunities for novel and impactful psychoneuroimmunology (PNI) research to enhance health outcomes, quality of life, and longevity among both MM patients and their caregivers.
    Language English
    Publishing date 2024-04-21
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 639219-2
    ISSN 1090-2139 ; 0889-1591
    ISSN (online) 1090-2139
    ISSN 0889-1591
    DOI 10.1016/j.bbi.2024.04.019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: A dyadic longitudinal analysis of parent-adolescent inflammation trends and the role of shared socioeconomic characteristics on family inflammation.

    Rocha, Sarah / Bower, Julienne E / Chiang, Jessica J / Cole, Steve W / Irwin, Michael R / Seeman, Teresa / Fuligni, Andrew J

    Brain, behavior, & immunity - health

    2024  Volume 38, Page(s) 100767

    Abstract: The objective of the present study was to evaluate the interdependency of parent-adolescent inflammation trends across time and to examine whether shared family socioeconomic characteristics explained between-family differences in parents' and ... ...

    Abstract The objective of the present study was to evaluate the interdependency of parent-adolescent inflammation trends across time and to examine whether shared family socioeconomic characteristics explained between-family differences in parents' and adolescents' risk for inflammation. A total of N = 348 families, consisting of one parent and one adolescent child, were followed every two years in a three-wave longitudinal study. Sociodemographic questionnaires were used to determine parental educational attainment and family income-to-needs ratio (INR). At each time point, parents and adolescents collected dried blood spot (DBS) samples that were assayed for circulating CRP and log-transformed prior to analysis by longitudinal dyadic models. Models revealed significant differences in parents' and adolescents' inflammation trends over time (b
    Language English
    Publishing date 2024-04-04
    Publishing country United States
    Document type Journal Article
    ISSN 2666-3546
    ISSN (online) 2666-3546
    DOI 10.1016/j.bbih.2024.100767
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  10. Article: Accelerated epigenetic aging mediates link between adverse childhood experiences and depressive symptoms in older adults: Results from the Health and Retirement Study.

    Klopack, Eric T / Crimmins, Eileen M / Cole, Steve W / Seeman, Teresa E / Carroll, Judith E

    SSM - population health

    2022  Volume 17, Page(s) 101071

    Abstract: Adverse childhood experiences (ACEs) increase risk for depression at subsequent ages and have been linked to accelerated biological aging. We hypothesize that accelerated epigenetic aging may partially mediate the link between ACEs and depression. This ... ...

    Abstract Adverse childhood experiences (ACEs) increase risk for depression at subsequent ages and have been linked to accelerated biological aging. We hypothesize that accelerated epigenetic aging may partially mediate the link between ACEs and depression. This study examines 3 three second-generation epigenetic aging measures (viz., GrimAge, PhenoAge, and DunedinPoAm38) as mediators of the link between ACEs and depressive symptoms in older adulthood. We utilize structural equation modeling to assess mediation in the Health and Retirement Study (N = 2672). Experiencing ACEs is significantly associated with an older GrimAge and a faster pace of aging via the DunedinPoAm38. Having an older GrimAge and faster DunedinPoAm38 pace of aging were also significantly associated with more depressive symptoms. PhenoAge was not significantly associated with depressive symptoms and was only associated with experiencing three ACEs. These associations were reduced by socioeconomic and lifestyle factors, including obesity and substance use. GrimAge explained between 9 and 14% of the association between ACEs and adult depressive symptoms, and DunedinPoAm38 explained between 2 and 7% of the association between ACEs and adult depressive symptoms. Findings indicate accelerated aging, as measured by GrimAge and DunedinPoAm38, is associated with ACEs and with depressive symptoms in older Americans. Findings also show these epigenetic aging measures mediate a portion of the association between ACEs and adult depressive symptoms. Epigenetic aging may represent a physiological mechanism underlying the link between early life adversity and adult depression. Weight maintenance and substance use are potentially important areas for intervention.
    Language English
    Publishing date 2022-03-16
    Publishing country England
    Document type Journal Article
    ISSN 2352-8273
    ISSN 2352-8273
    DOI 10.1016/j.ssmph.2022.101071
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