Exploring joint HPA-inflammatory stress response profiles in adolescent girls: Implications for developmental models of neuroendocrine dysregulation.

Exploring joint HPA-inflammatory stress response profiles in adolescent girls: Implications for developmental models of neuroendocrine dysregulation.
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DOI:
10.1002/dev.22247
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发表时间:
2022-03
影响因子:
2.2
通讯作者:
Prinstein MJ
Prinstein MJ
中科院分区:
心理学4区
文献类型:
--
作者:
Bendezú JJ;Calhoun CD;Vinograd M;Patterson MW;Rudolph KD;Giletta M;Hastings P;Nock MK;Slavich GM;Prinstein MJ

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先前的研究一直在努力区分皮质醇应激反应模式,反映青少年下丘脑-垂体-肾上腺(HPA)轴功能调节良好与失调。在这里,我们展示了如何探索联合HPA炎症应激反应的配置文件,并将这些配置文件与青春期发育和同龄人的压力暴露,可能有助于这种区分。有精神病理学风险的青春期女孩(N=157,法师=14.72岁,SD=1.38)完成了唾液皮质醇和促炎细胞因子(即,肿瘤坏死因子-α、白细胞介素-1 β和白细胞介素-6)。青少年,一个亲密的朋友,和照顾者完成了同伴压力和青春期状态的问卷测量。青少年皮质醇和细胞因子水平的多轨迹模型显示了三种特征:低皮质醇反应-稳定低细胞因子(n=75),高皮质醇反应-稳定中等细胞因子(n=47)和低皮质醇反应-稳定高细胞因子(n=35)。相对于低皮质醇反应-稳定低细胞因子,表现出高皮质醇反应-稳定中等细胞因子特征的青少年在青春期发育中更先进,但表现出类似的低水平的同伴压力暴露。尽管表现出皮质醇反应与低皮质醇反应-稳定低细胞因子无法区分,但表现出低皮质醇反应-稳定高细胞因子特征的青少年更接近青春期,但也更有可能经历慢性同伴压力(自我报告)和关系同伴受害(亲密朋友报告)。因此,这些研究结果说明了潜在的价值,采取多系统的方法来研究青少年的压力反应,并强调在解释皮质醇压力反应模式时考虑发展和社会因素的重要性。最终,这些工作可能有助于为神经内分泌失调和精神病理学相关风险的发育模型提供信息。
Prior research has struggled to differentiate cortisol stress response patterns reflective of well-regulated versus dysregulated hypothalamic-pituitary-adrenal (HPA) axis function among adolescents. Here, we show how exploring profiles of joint HPA–inflammatory stress responsivity, and linking those profiles to pubertal development and peer stress exposure, may aid such distinction. Adolescent girls (N=157, Mage=14.72 years, SD=1.38) at risk for psychopathology completed assessments of salivary cortisol and pro-inflammatory cytokines (i.e., tumor necrosis factor-α, interleukin-1β, and interleukin-6) prior to and following the Trier Social Stress Test. Adolescents, a close friend, and a caregiver completed questionnaire measures of peer stress and pubertal status. Multitrajectory modeling of adolescents’ cortisol and cytokine levels revealed three profiles: Low Cortisol Response–Stably Low Cytokine (n=75), High Cortisol Response–Stably Moderate Cytokine (n=47), and Low Cortisol Response–Stably High Cytokine (n=35). Relative to Low Cortisol Response–Stably Low Cytokine, adolescents exhibiting the High Cortisol Response–Stably Moderate Cytokine profile were more advanced in their pubertal development, but presented with similarly low levels of peer stress exposure. Despite showing cortisol responses that were indistinguishable from Low Cortisol Response–Stably Low Cytokine, adolescents exhibiting the Low Cortisol Response–Stably High Cytokine profile were more pubertally advanced, but also more likely to have experienced chronic peer strain (self-report) and relational peer victimization (close friend-report). These findings thus illustrate the potential value of taking a multisystem approach to studying adolescent stress responsivity and underscore the importance of considering developmental and social factors when interpreting cortisol stress response patterns. Ultimately, such work may help inform developmental models of neuroendocrine dysregulation and related risk for psychopathology.
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