Chronic interpersonal stress predicts activation of pro- and anti-inflammatory signaling pathways 6 months later.
Chronic interpersonal stress predicts activation of pro- and anti-inflammatory signaling pathways 6 months later.
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DOI：
10.1097/psy.0b013e318190d7de
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发表时间：
2009-01
影响因子：
3.3
通讯作者：
Cole SW
中科院分区：
文献类型：
--
作者：
Miller GE;Rohleder N;Cole SW
慢性人际交往困难对身心健康有不利影响，但对这种现象背后的机制知之甚少。103名健康年轻女性（平均年龄= 17岁）进行了结构化访谈，以评估其生活中的慢性人际压力程度。与此同时，抽取血液以测量全身炎症、调节免疫活化的信号分子的表达以及在用脂多糖离体刺激后白细胞产生细胞因子白细胞介素-6。6个月后重复所有免疫学评估。受试者在基线时慢性人际压力较高，在接下来的六个月里，他们的白细胞显示出促炎转录因子核因子-κ B（NF-κB）mRNA的更大增加。它们还显示出kappaB抑制剂的mRNA的较大增加，kappaB是一种在细胞质中隔离NF-κB并使其促炎活性最小化的分子。慢性人际压力在基线时与全身炎症生物标志物的变化无关，但与白细胞介素-6对脂多糖的反应越来越明显有关。这些关联与人口统计学、生活方式变量和抑郁症状无关。这些发现表明，慢性人际交往困难加重了促炎和抗炎信号分子的表达。虽然该过程在静止条件下不会导致全身性炎症，但它确实加重了白细胞对微生物挑战的炎症反应。这些动力学可能是与社会压力相关的过度发病率的基础，特别是在抑郁症和动脉粥样硬化等炎症敏感性疾病中。
Chronic interpersonal difficulties have a detrimental influence on mental and physical health, but little is known about the mechanisms underlying this phenomenon. 103 healthy young women (mean age = 17) were administered a structured interview to assess the degree of chronic interpersonal stress in their lives. At the same time blood was drawn to measure systemic inflammation, the expression of signaling molecules that regulate immune activation, and leukocyte production of the cytokine interleukin-6 following ex vivo stimulation with lipopolysaccharide. All of the immunologic assessments were repeated six months later. To the extent subjects were high in chronic interpersonal stress at baseline, their leukocytes displayed greater increases in mRNA for the pro-inflammatory transcription factor nuclear factor-kappa B (NF-κB) over the next six months. They also showed larger increases in mRNA for inhibitor of kappaB, a molecule that sequesters NF-κB in the cytoplasm and minimizes its pro-inflammatory activities. Chronic interpersonal stress at baseline was unrelated to changes in biomarkers of systemic inflammation, but was associated with increasingly pronounced interleukin-6 responses to lipopolysaccharide. These associations were independent of demographics, lifestyle variables, and depressive symptoms. These findings suggest that chronic interpersonal difficulties accentuate expression of pro- and anti-inflammatory signaling molecules. While this process does not result in systemic inflammation under quiescent conditions, it does accentuate leukocytes’ inflammatory response to microbial challenge. These dynamics may underlie the excess morbidity associated with social stress, particularly in inflammation-sensitive diseases like depression and atherosclerosis.