Nathalie Michels , Thomas W. McDade , Keegan C. Krause , Aaron A. Miller , Matteo Giletta
{"title":"社会逆境的历史与青少年的体外炎症反应有关","authors":"Nathalie Michels , Thomas W. McDade , Keegan C. Krause , Aaron A. Miller , Matteo Giletta","doi":"10.1016/j.psyneuen.2025.107620","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Social adversity is consistently associated with negative mental and physical health outcomes, potentially through dysregulated inflammatory processes. Adolescence is a critical period for these effects to emerge. Traditional baseline measures of chronic inflammation often fail to capture the dynamic nature of inflammatory responses, highlighting the importance of assessing both inflammatory reactivity and sensitivity to inhibition. This study examined whether a history of social adversity predicts adolescents’ <em>ex vivo</em> inflammatory responses.</div></div><div><h3>Methods</h3><div>As part of the longitudinal Outside-in study, 333 Belgian adolescents (13.9 ± 0.4 years, 44.1 % girls) provided blood samples via fingerprick in a school setting. Blood was incubated with lipopolysaccharide to assess inflammatory reactivity, and with lipopolysaccharide plus glucocorticoid (GC) to assess GC sensitivity. Cytokine responses were measured for IL-1β, IL-6, and TNF-α. Social adversity, assessed through self-reported bullying victimization and victimization by adults over four waves spanning two years, was used as a predictor. Linear regression models adjusted for sex, pubertal status, and infection-related symptoms, while accounting for multiple testing.</div></div><div><h3>Results</h3><div>A two-year history of social adversity predicted IL-6 (β=0.119) and TNF-α (β=0.123) reactivity but not GC sensitivity or IL-1β reactivity. Similar patterns were observed for concurrent social adversity and for the two types of adversity analyzed separately.</div></div><div><h3>Conclusion</h3><div>In this community sample of adolescents, social adversity was associated with heightened inflammatory reactivity of TNF-α and IL-6. This increased reactivity might put adolescents at risk of developing chronic low-grade inflammation over time.</div></div>","PeriodicalId":20836,"journal":{"name":"Psychoneuroendocrinology","volume":"182 ","pages":"Article 107620"},"PeriodicalIF":3.6000,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A history of social adversity is associated with adolescents’ ex vivo inflammatory response\",\"authors\":\"Nathalie Michels , Thomas W. McDade , Keegan C. Krause , Aaron A. Miller , Matteo Giletta\",\"doi\":\"10.1016/j.psyneuen.2025.107620\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><div>Social adversity is consistently associated with negative mental and physical health outcomes, potentially through dysregulated inflammatory processes. Adolescence is a critical period for these effects to emerge. Traditional baseline measures of chronic inflammation often fail to capture the dynamic nature of inflammatory responses, highlighting the importance of assessing both inflammatory reactivity and sensitivity to inhibition. This study examined whether a history of social adversity predicts adolescents’ <em>ex vivo</em> inflammatory responses.</div></div><div><h3>Methods</h3><div>As part of the longitudinal Outside-in study, 333 Belgian adolescents (13.9 ± 0.4 years, 44.1 % girls) provided blood samples via fingerprick in a school setting. Blood was incubated with lipopolysaccharide to assess inflammatory reactivity, and with lipopolysaccharide plus glucocorticoid (GC) to assess GC sensitivity. Cytokine responses were measured for IL-1β, IL-6, and TNF-α. Social adversity, assessed through self-reported bullying victimization and victimization by adults over four waves spanning two years, was used as a predictor. Linear regression models adjusted for sex, pubertal status, and infection-related symptoms, while accounting for multiple testing.</div></div><div><h3>Results</h3><div>A two-year history of social adversity predicted IL-6 (β=0.119) and TNF-α (β=0.123) reactivity but not GC sensitivity or IL-1β reactivity. Similar patterns were observed for concurrent social adversity and for the two types of adversity analyzed separately.</div></div><div><h3>Conclusion</h3><div>In this community sample of adolescents, social adversity was associated with heightened inflammatory reactivity of TNF-α and IL-6. This increased reactivity might put adolescents at risk of developing chronic low-grade inflammation over time.</div></div>\",\"PeriodicalId\":20836,\"journal\":{\"name\":\"Psychoneuroendocrinology\",\"volume\":\"182 \",\"pages\":\"Article 107620\"},\"PeriodicalIF\":3.6000,\"publicationDate\":\"2025-09-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Psychoneuroendocrinology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0306453025003439\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Psychoneuroendocrinology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0306453025003439","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
A history of social adversity is associated with adolescents’ ex vivo inflammatory response
Background
Social adversity is consistently associated with negative mental and physical health outcomes, potentially through dysregulated inflammatory processes. Adolescence is a critical period for these effects to emerge. Traditional baseline measures of chronic inflammation often fail to capture the dynamic nature of inflammatory responses, highlighting the importance of assessing both inflammatory reactivity and sensitivity to inhibition. This study examined whether a history of social adversity predicts adolescents’ ex vivo inflammatory responses.
Methods
As part of the longitudinal Outside-in study, 333 Belgian adolescents (13.9 ± 0.4 years, 44.1 % girls) provided blood samples via fingerprick in a school setting. Blood was incubated with lipopolysaccharide to assess inflammatory reactivity, and with lipopolysaccharide plus glucocorticoid (GC) to assess GC sensitivity. Cytokine responses were measured for IL-1β, IL-6, and TNF-α. Social adversity, assessed through self-reported bullying victimization and victimization by adults over four waves spanning two years, was used as a predictor. Linear regression models adjusted for sex, pubertal status, and infection-related symptoms, while accounting for multiple testing.
Results
A two-year history of social adversity predicted IL-6 (β=0.119) and TNF-α (β=0.123) reactivity but not GC sensitivity or IL-1β reactivity. Similar patterns were observed for concurrent social adversity and for the two types of adversity analyzed separately.
Conclusion
In this community sample of adolescents, social adversity was associated with heightened inflammatory reactivity of TNF-α and IL-6. This increased reactivity might put adolescents at risk of developing chronic low-grade inflammation over time.
期刊介绍:
Psychoneuroendocrinology publishes papers dealing with the interrelated disciplines of psychology, neurobiology, endocrinology, immunology, neurology, and psychiatry, with an emphasis on multidisciplinary studies aiming at integrating these disciplines in terms of either basic research or clinical implications. One of the main goals is to understand how a variety of psychobiological factors interact in the expression of the stress response as it relates to the development and/or maintenance of neuropsychiatric illnesses.