Subjective social status and inflammatory gene expression

主观社会地位与炎症基因表达

阅读:1

Abstract

OBJECTIVE: There exists a well-established link between low perceived social status and poorer health outcomes. However, the molecular mechanisms associated with this link remain unclear. This study begins to fill this gap by investigating the effects of low perceived subjective social status on health-related gene expression. METHOD: Participants were 47 healthy heterosexual women (mean age 20.5 years) from a large American university. Participants gave 10 mL of peripheral blood and completed questionnaires assessing subjective social status (SSS), perceived childhood socioeconomic status (SES), health, and relevant demographics. Putatively associated genes were subject to TELiS promoter-based bioinformatic analysis to assess activity of proinflammatory, anti-inflammatory, and antiviral transcription factors. RESULTS: In analyses controlling for perceived childhood socioeconomic status (SES) and other covariates, 84 transcripts showed >1.5-fold difference in average expression across the range of SSS. TELiS bioinformatics analyses implicated the proinflammatory transcription factors, NF-κB and AP-1, in driving expression of genes that were up-regulated in low-SSS individuals. Results also indicated increased activity of CREB family transcription factors but no differential activity of the anti-inflammatory glucocorticoid receptor of interferon response factors. Transcript origin analysis implicated monocytes and dendritic cells as cellular mediators. CONCLUSION: In this first study examining the molecular correlates of SSS, experiences of low social status are associated with transcriptional effects similar to those previously observed for objective adversity conditions such as low SES, social isolation, and chronic stress. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。