School of Medicine, University of California, Los Angeles, CA 90095;
Norman Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience & Human Behavior, University of California, Los Angeles, CA 90095.
Proc Natl Acad Sci U S A. 2020 Mar 3;117(9):4601-4608. doi: 10.1073/pnas.1821367117. Epub 2020 Feb 10.
Health in later life varies significantly by individual demographic characteristics such as age, sex, and race/ethnicity, as well as by social factors including socioeconomic status and geographic region. This study examined whether sociodemographic variations in the immune and inflammatory molecular underpinnings of chronic disease might emerge decades earlier in young adulthood. Using data from 1,069 young adults from the National Longitudinal Study of Adolescent to Adult Health (Add Health)-the largest nationally representative and ethnically diverse sample with peripheral blood transcriptome profiles-we analyzed variation in the expression of genes involved in inflammation and type I interferon (IFN) response as a function of individual demographic factors, sociodemographic conditions, and biobehavioral factors (smoking, drinking, and body mass index). Differential gene expression was most pronounced by sex, race/ethnicity, and body mass index (BMI), but transcriptome correlates were identified for every demographic dimension analyzed. Inflammation-related gene expression showed the most pronounced variation as a function of biobehavioral factors (BMI and smoking) whereas type I IFN-related transcripts varied most strongly as a function of individual demographic characteristics (sex and race/ethnicity). Bioinformatic analyses of transcription factor and immune-cell activation based on transcriptome-wide empirical differences identified additional effects of family poverty and geographic region. These results identify pervasive sociodemographic differences in immune-cell gene regulation that emerge by young adulthood and may help explain social disparities in the development of chronic illness and premature mortality at older ages.
健康在晚年有很大的差异，这取决于个体的人口特征，如年龄、性别和种族/民族，以及社会因素，包括社会经济地位和地理位置。本研究探讨了慢性疾病的免疫和炎症分子基础是否会在成年早期几十年前就因社会人口因素而出现差异。该研究使用了来自国家青少年到成人健康纵向研究（Add Health）的 1069 名年轻人的数据——这是一个最大的全国代表性和种族多样化的外周血转录组谱样本，分析了炎症和 I 型干扰素（IFN）反应相关基因表达的个体人口因素、社会人口状况和生物行为因素（吸烟、饮酒和体重指数）的变化。基因表达的差异在性别、种族/民族和体重指数（BMI）方面最为明显，但分析的每一个人口维度都确定了转录组相关因素。炎症相关基因表达的变化最明显的是生物行为因素（BMI 和吸烟），而 I 型 IFN 相关转录物的变化最明显的是个体人口特征（性别和种族/民族）。基于转录组全经验差异的转录因子和免疫细胞激活的生物信息学分析，还确定了家庭贫困和地理位置的额外影响。这些结果表明，免疫细胞基因调控存在普遍的社会人口差异，这种差异在成年早期就出现了，可能有助于解释在老年时期慢性疾病和过早死亡的社会差异。
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