Adverse childhood experiences and transcriptional response in school-age children / A. MARIE-MITCHELL in Development and Psychopathology, 34-3 (August 2022)  

Public ISBD [article]  inDevelopment and Psychopathology > 34-3 (August 2022) . - p.875-881 Titre : Adverse childhood experiences and transcriptional response in school-age children Type de document : texte imprimé Auteurs : A. MARIE-MITCHELL, Auteur ; Steven W. COLE, Auteur Article en page(s) : p.875-881 Langues : Anglais (eng) Mots-clés : adverse childhood experiences  adversity  biomarkers  immunology  inflammation Index. décimale : PER Périodiques Résumé : This study evaluated whether children with higher adverse childhood experiences (ACE) scores had alterations in immune cell gene expression profiles. RNA sequencing was conducted on dried blood spot samples from 37 generally healthy English-speaking children (age 5 “11) who were recruited from well-child visits at a university-affiliated pediatric practice. The Whole Child Assessment was used to assess ACE exposure. Primary analyses examined an a priori-specified composite of 19 pro-inflammatory gene transcripts. Secondary analyses examined a 34-gene composite assessing Type I interferon response, and used Transcript Origin Analyses to identify cellular mechanisms. After controlling for age, body mass index percentile, sex, race/ethnicity, current insurance status, and household smoking exposure, pro-inflammatory gene expression was elevated by 0.094 log2 RNA expression units with each Child-ACE total score point (p = .019). Type I interferon gene expression was similarly upregulated (0.103; p = .008). Transcript origin analyses implicated CD8+ T cell as the primary sources of gene transcripts upregulated, and nonclassical (CD16+) monocytes as sources of downregulated transcripts. These preliminary analyses suggest that parent-reported ACE exposures are associated with increased expression of both inflammatory and interferon gene transcripts in children's circulating blood cells. En ligne : http://dx.doi.org/10.1017/S095457942000187X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=484 [article] Adverse childhood experiences and transcriptional response in school-age children [texte imprimé] / A. MARIE-MITCHELL, Auteur ; Steven W. COLE, Auteur . - p.875-881. Langues : Anglais (eng) in Development and Psychopathology > 34-3 (August 2022) . - p.875-881 Mots-clés : adverse childhood experiences  adversity  biomarkers  immunology  inflammation Index. décimale : PER Périodiques Résumé : This study evaluated whether children with higher adverse childhood experiences (ACE) scores had alterations in immune cell gene expression profiles. RNA sequencing was conducted on dried blood spot samples from 37 generally healthy English-speaking children (age 5 “11) who were recruited from well-child visits at a university-affiliated pediatric practice. The Whole Child Assessment was used to assess ACE exposure. Primary analyses examined an a priori-specified composite of 19 pro-inflammatory gene transcripts. Secondary analyses examined a 34-gene composite assessing Type I interferon response, and used Transcript Origin Analyses to identify cellular mechanisms. After controlling for age, body mass index percentile, sex, race/ethnicity, current insurance status, and household smoking exposure, pro-inflammatory gene expression was elevated by 0.094 log2 RNA expression units with each Child-ACE total score point (p = .019). Type I interferon gene expression was similarly upregulated (0.103; p = .008). Transcript origin analyses implicated CD8+ T cell as the primary sources of gene transcripts upregulated, and nonclassical (CD16+) monocytes as sources of downregulated transcripts. These preliminary analyses suggest that parent-reported ACE exposures are associated with increased expression of both inflammatory and interferon gene transcripts in children's circulating blood cells. En ligne : http://dx.doi.org/10.1017/S095457942000187X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=484

Family environments and leukocyte transcriptome indicators of a proinflammatory phenotype in children and parents / Theodore F. ROBLES in Development and Psychopathology, 30-1 (February 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-1 (February 2018) . - p.235-253 Titre : Family environments and leukocyte transcriptome indicators of a proinflammatory phenotype in children and parents Type de document : texte imprimé Auteurs : Theodore F. ROBLES, Auteur ; Rena L. REPETTI, Auteur ; Bridget REYNOLDS, Auteur ; Paul J. CHUNG, Auteur ; Jesusa M.G. AREVALO, Auteur ; Steven W. COLE, Auteur Article en page(s) : p.235-253 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : High conflict and low warmth in families may contribute to immune cells developing a tendency to respond to threats with exaggerated inflammation that is insensitive to inhibitory signaling. We tested associations between family environments and expression of genes bearing response elements for transcription factors that regulate inflammation: nuclear factor kappa B (NF-κB) and glucocorticoid receptor. The overall sample (47 families) completed interviews, questionnaires, and 8-week daily diary assessments of conflict and warmth, which were used to create composite family conflict and warmth scores. The diaries assessed upper respiratory infection (URI) symptoms, and URI episodes were clinically verified. Leukocyte RNA was extracted from whole blood samples provided by a subsample of 42 children (8–13 years of age) and 73 parents. In children, higher conflict and lower warmth were related to greater expression of genes bearing response elements for the proinflammatory transcription factor NF-κB, and more severe URI symptoms. In parents, higher conflict and lower warmth were also related to greater NF-κB–associated gene expression. Monocytes and dendritic cells were implicated as primary cellular sources of differential gene expression in the sample. Consistent with existing conceptual frameworks, stressful family environments were related to a proinflammatory phenotype at the level of the circulating leukocyte transcriptome. En ligne : https://doi.org/10.1017/S0954579417000591 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=336 [article] Family environments and leukocyte transcriptome indicators of a proinflammatory phenotype in children and parents [texte imprimé] / Theodore F. ROBLES, Auteur ; Rena L. REPETTI, Auteur ; Bridget REYNOLDS, Auteur ; Paul J. CHUNG, Auteur ; Jesusa M.G. AREVALO, Auteur ; Steven W. COLE, Auteur . - p.235-253. Langues : Anglais (eng) in Development and Psychopathology > 30-1 (February 2018) . - p.235-253 Index. décimale : PER Périodiques Résumé : High conflict and low warmth in families may contribute to immune cells developing a tendency to respond to threats with exaggerated inflammation that is insensitive to inhibitory signaling. We tested associations between family environments and expression of genes bearing response elements for transcription factors that regulate inflammation: nuclear factor kappa B (NF-κB) and glucocorticoid receptor. The overall sample (47 families) completed interviews, questionnaires, and 8-week daily diary assessments of conflict and warmth, which were used to create composite family conflict and warmth scores. The diaries assessed upper respiratory infection (URI) symptoms, and URI episodes were clinically verified. Leukocyte RNA was extracted from whole blood samples provided by a subsample of 42 children (8–13 years of age) and 73 parents. In children, higher conflict and lower warmth were related to greater expression of genes bearing response elements for the proinflammatory transcription factor NF-κB, and more severe URI symptoms. In parents, higher conflict and lower warmth were also related to greater NF-κB–associated gene expression. Monocytes and dendritic cells were implicated as primary cellular sources of differential gene expression in the sample. Consistent with existing conceptual frameworks, stressful family environments were related to a proinflammatory phenotype at the level of the circulating leukocyte transcriptome. En ligne : https://doi.org/10.1017/S0954579417000591 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=336

Proinflammatory gene expression is associated with prospective risk for adolescent suicidal thoughts and behaviors over twelve months / Matthew G. CLAYTON in Development and Psychopathology, 37-3 (August 2025)  

Public ISBD [article]  inDevelopment and Psychopathology > 37-3 (August 2025) . - p.1676-1684 Titre : Proinflammatory gene expression is associated with prospective risk for adolescent suicidal thoughts and behaviors over twelve months Type de document : texte imprimé Auteurs : Matthew G. CLAYTON, Auteur ; Steven W. COLE, Auteur ; Matteo GILETTA, Auteur ; Paul D. HASTINGS, Auteur ; Matthew K. NOCK, Auteur ; Karen D. RUDOLPH, Auteur ; George M. SLAVICH, Auteur ; Mitchell J. PRINSTEIN, Auteur Article en page(s) : p.1676-1684 Langues : Anglais (eng) Mots-clés : adolescence  biomarkers  childhood trauma  inflammation  suicide Index. décimale : PER Périodiques Résumé : Objective:Recent theories have implicated inflammatory biology in the development of psychopathology and maladaptive behaviors in adolescence, including suicidal thoughts and behaviors (STB). Examining specific biological markers related to inflammation is thus warranted to better understand risk for STB in adolescents, for whom suicide is a leading cause of death.Method:Participants were 211 adolescent females (ages 9-14 years; Mage = 11.8 years, SD = 1.8 years) at increased risk for STB. This study examined the prospective association between basal levels of inflammatory gene expression (average of 15 proinflammatory mRNA transcripts) and subsequent risk for suicidal ideation and suicidal behavior over a 12-month follow-up period.Results:Controlling for past levels of STB, greater proinflammatory gene expression was associated with prospective risk for STB in these youth. Similar effects were observed for CD14 mRNA level, a marker of monocyte abundance within the blood sample. Sensitivity analyses controlling for other relevant covariates, including history of trauma, depressive symptoms, and STB prior to data collection, yielded similar patterns of results.Conclusions:Upregulated inflammatory signaling in the immune system is prospectively associated with STB among at-risk adolescent females, even after controlling for history of trauma, depressive symptoms, and STB prior to data collection. Additional research is needed to identify the sources of inflammatory up-regulation in adolescents (e.g., stress psychobiology, physiological development, microbial exposures) and strategies for mitigating such effects to reduce STB. En ligne : https://www.cambridge.org/core/product/25AD4CF3A7BD16D263771246B7E45F56 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=564 [article] Proinflammatory gene expression is associated with prospective risk for adolescent suicidal thoughts and behaviors over twelve months [texte imprimé] / Matthew G. CLAYTON, Auteur ; Steven W. COLE, Auteur ; Matteo GILETTA, Auteur ; Paul D. HASTINGS, Auteur ; Matthew K. NOCK, Auteur ; Karen D. RUDOLPH, Auteur ; George M. SLAVICH, Auteur ; Mitchell J. PRINSTEIN, Auteur . - p.1676-1684. Langues : Anglais (eng) in Development and Psychopathology > 37-3 (August 2025) . - p.1676-1684 Mots-clés : adolescence  biomarkers  childhood trauma  inflammation  suicide Index. décimale : PER Périodiques Résumé : Objective:Recent theories have implicated inflammatory biology in the development of psychopathology and maladaptive behaviors in adolescence, including suicidal thoughts and behaviors (STB). Examining specific biological markers related to inflammation is thus warranted to better understand risk for STB in adolescents, for whom suicide is a leading cause of death.Method:Participants were 211 adolescent females (ages 9-14 years; Mage = 11.8 years, SD = 1.8 years) at increased risk for STB. This study examined the prospective association between basal levels of inflammatory gene expression (average of 15 proinflammatory mRNA transcripts) and subsequent risk for suicidal ideation and suicidal behavior over a 12-month follow-up period.Results:Controlling for past levels of STB, greater proinflammatory gene expression was associated with prospective risk for STB in these youth. Similar effects were observed for CD14 mRNA level, a marker of monocyte abundance within the blood sample. Sensitivity analyses controlling for other relevant covariates, including history of trauma, depressive symptoms, and STB prior to data collection, yielded similar patterns of results.Conclusions:Upregulated inflammatory signaling in the immune system is prospectively associated with STB among at-risk adolescent females, even after controlling for history of trauma, depressive symptoms, and STB prior to data collection. Additional research is needed to identify the sources of inflammatory up-regulation in adolescents (e.g., stress psychobiology, physiological development, microbial exposures) and strategies for mitigating such effects to reduce STB. En ligne : https://www.cambridge.org/core/product/25AD4CF3A7BD16D263771246B7E45F56 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=564

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