Examining systemic inflammation as a pathway linking peer victimization to depressive symptoms in adolescence / Nathalie MICHELS ; George M. SLAVICH ; Matteo GILETTA in Journal of Child Psychology and Psychiatry, 66-3 (March 2025)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 66-3 (March 2025) . - p.311-321 Titre : Examining systemic inflammation as a pathway linking peer victimization to depressive symptoms in adolescence Type de document : Texte imprimé et/ou numérique Auteurs : Nathalie MICHELS, Auteur ; George M. SLAVICH, Auteur ; Matteo GILETTA, Auteur Article en page(s) : p.311-321 Langues : Anglais (eng) Mots-clés : Adolescence  depression  inflammation  interleukin-6  peer victimization  social stress Index. décimale : PER Périodiques Résumé : Background Adolescents exposed to victimization are at an increased risk for a variety of adverse mental health outcomes, including depressive symptoms. Yet, the biological pathways underlying these associations remain poorly understood. Focusing on within-person processes, we examined whether low-grade systemic inflammation mediated the longitudinal associations between peer victimization and depressive symptoms in adolescence. Methods 207 adolescents (at baseline Mage?=?12.69?years; SD?=?0.49; 43.5% female) participated in a multi-wave longitudinal study, with assessments repeated every 6?months over 1.5?years. At each assessment wave, participants self-reported their peer victimization experiences and depressive symptoms. Dried blood spots were collected at each wave using a finger prick procedure to assay a key marker of low-grade systemic inflammation, interkeukin-6 (IL-6). Data were analyzed using random-intercept cross-lagged panel models. Results The cross-lagged paths from IL-6 to depressive symptoms were significant across all models and waves (?12?=?.13; ?23?=?.12; ?34?=?.08), indicating that when adolescents' levels of low-grade systemic inflammation were above their person-specific average, they reported increased levels of depressive symptoms in the subsequent months. However, no significant cross-lagged within-person associations emerged between peer victimization and either IL-6 or depressive symptoms. Conclusions The findings provide no evidence for the hypothesized mediating role of inflammation in the within-person associations between peer victimization and depressive symptoms. Nevertheless, they extend prior research by indicating that elevated levels of low-grade systemic inflammation predict the development of depressive symptoms in adolescence. En ligne : https://doi.org/10.1111/jcpp.14060 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=548 [article] Examining systemic inflammation as a pathway linking peer victimization to depressive symptoms in adolescence [Texte imprimé et/ou numérique] / Nathalie MICHELS, Auteur ; George M. SLAVICH, Auteur ; Matteo GILETTA, Auteur . - p.311-321. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 66-3 (March 2025) . - p.311-321 Mots-clés : Adolescence  depression  inflammation  interleukin-6  peer victimization  social stress Index. décimale : PER Périodiques Résumé : Background Adolescents exposed to victimization are at an increased risk for a variety of adverse mental health outcomes, including depressive symptoms. Yet, the biological pathways underlying these associations remain poorly understood. Focusing on within-person processes, we examined whether low-grade systemic inflammation mediated the longitudinal associations between peer victimization and depressive symptoms in adolescence. Methods 207 adolescents (at baseline Mage?=?12.69?years; SD?=?0.49; 43.5% female) participated in a multi-wave longitudinal study, with assessments repeated every 6?months over 1.5?years. At each assessment wave, participants self-reported their peer victimization experiences and depressive symptoms. Dried blood spots were collected at each wave using a finger prick procedure to assay a key marker of low-grade systemic inflammation, interkeukin-6 (IL-6). Data were analyzed using random-intercept cross-lagged panel models. Results The cross-lagged paths from IL-6 to depressive symptoms were significant across all models and waves (?12?=?.13; ?23?=?.12; ?34?=?.08), indicating that when adolescents' levels of low-grade systemic inflammation were above their person-specific average, they reported increased levels of depressive symptoms in the subsequent months. However, no significant cross-lagged within-person associations emerged between peer victimization and either IL-6 or depressive symptoms. Conclusions The findings provide no evidence for the hypothesized mediating role of inflammation in the within-person associations between peer victimization and depressive symptoms. Nevertheless, they extend prior research by indicating that elevated levels of low-grade systemic inflammation predict the development of depressive symptoms in adolescence. En ligne : https://doi.org/10.1111/jcpp.14060 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=548

Peer victimization predicts heightened inflammatory reactivity to social stress in cognitively vulnerable adolescents / Matteo GILETTA in Journal of Child Psychology and Psychiatry, 59-2 (February 2018)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 59-2 (February 2018) . - p.129-139 Titre : Peer victimization predicts heightened inflammatory reactivity to social stress in cognitively vulnerable adolescents Type de document : Texte imprimé et/ou numérique Auteurs : Matteo GILETTA, Auteur ; George M. SLAVICH, Auteur ; Karen D. RUDOLPH, Auteur ; Paul D. HASTINGS, Auteur ; Matthew K. NOCK, Auteur ; Mitchell J. PRINSTEIN, Auteur Article en page(s) : p.129-139 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Background During adolescence, peer victimization is a potent type of social stressor that can confer enduring risk for poor mental and physical health. Given recent research implicating inflammation in promoting a variety of serious mental and physical health problems, this study examined the role that peer victimization and cognitive vulnerability (i.e. negative cognitive styles and hopelessness) play in shaping adolescents’ pro?inflammatory cytokine responses to an acute social stressor. Methods Adolescent girls at risk for psychopathology (n = 157; Mage = 14.73 years; SD = 1.38) were exposed to a laboratory?based social stressor before and after which we assessed salivary levels of three key pro?inflammatory cytokines – interleukin?6 (IL?6), interleukin?1? (IL?1?), and tumor necrosis factor?? (TNF??). Results As hypothesized, adolescents with greater peer victimization exposure exhibited greater increases in IL?6 and IL1?? in response to the laboratory?based social stressor. Moreover, for all three cytokines individually, as well as for a combined latent factor of inflammation, peer victimization predicted enhanced inflammatory responding most strongly for adolescents with high levels of hopelessness. Conclusions The findings reveal a biological pathway by which peer victimization may interact with cognitive vulnerability to influence health in adolescence. En ligne : https://doi.org/10.1111/jcpp.12804 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=339 [article] Peer victimization predicts heightened inflammatory reactivity to social stress in cognitively vulnerable adolescents [Texte imprimé et/ou numérique] / Matteo GILETTA, Auteur ; George M. SLAVICH, Auteur ; Karen D. RUDOLPH, Auteur ; Paul D. HASTINGS, Auteur ; Matthew K. NOCK, Auteur ; Mitchell J. PRINSTEIN, Auteur . - p.129-139. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 59-2 (February 2018) . - p.129-139 Index. décimale : PER Périodiques Résumé : Background During adolescence, peer victimization is a potent type of social stressor that can confer enduring risk for poor mental and physical health. Given recent research implicating inflammation in promoting a variety of serious mental and physical health problems, this study examined the role that peer victimization and cognitive vulnerability (i.e. negative cognitive styles and hopelessness) play in shaping adolescents’ pro?inflammatory cytokine responses to an acute social stressor. Methods Adolescent girls at risk for psychopathology (n = 157; Mage = 14.73 years; SD = 1.38) were exposed to a laboratory?based social stressor before and after which we assessed salivary levels of three key pro?inflammatory cytokines – interleukin?6 (IL?6), interleukin?1? (IL?1?), and tumor necrosis factor?? (TNF??). Results As hypothesized, adolescents with greater peer victimization exposure exhibited greater increases in IL?6 and IL1?? in response to the laboratory?based social stressor. Moreover, for all three cytokines individually, as well as for a combined latent factor of inflammation, peer victimization predicted enhanced inflammatory responding most strongly for adolescents with high levels of hopelessness. Conclusions The findings reveal a biological pathway by which peer victimization may interact with cognitive vulnerability to influence health in adolescence. En ligne : https://doi.org/10.1111/jcpp.12804 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=339

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 et/ou numérique Auteurs : Matthew G. CLAYTON, Auteur ; Steve 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 et/ou numérique] / Matthew G. CLAYTON, Auteur ; Steve 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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