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Linking stressful life events and chronic inflammation using suPAR (soluble urokinase plasminogen activator receptor)

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Kyle J. Bourassa, Line J.H. Rasmussen, Andrea Danese, Jesper Eugen-Olsen, Hona Lee Harrington, Renate Houts, Richie Poulton, Sandhya Ramrakha, Karen Sugden, Ben Williams, Terrie E. Moffitt, Avshalom Caspi

Original languageEnglish
Pages (from-to)79-88
Number of pages10
JournalBrain, Behavior, and Immunity
Volume97
DOIs
PublishedOct 2021

Bibliographical note

Funding Information: Note: The Dunedin Multidisciplinary Health and Development Research Unit is supported by the New Zealand Health Research Council and New Zealand Ministry of Business, Innovation and Employment (MBIE). The Dunedin Study received support from the US-National Institute on Aging [grants R01AG032282, P30AG028716, P30AG034424] and the UK Medical Research Council [grant MR/P005918/1]. KJB received support from the National Institute on Aging [grant T32-AG000029]. LJHR received support from the Lundbeck Foundation [grant R288-2018–380]. We thank the Dunedin Multidisciplinary Health and Development Study members, Unit research staff, and Study founder Phil Silva, PhD, University of Otago. The study’s preregistration materials can be accessed online at https://sites.google.com/site/moffittcaspiprojects/home/projectlist/bourassa_rasmussen_2019 . Publisher Copyright: © 2021 Elsevier Inc. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.

King's Authors

Abstract

Stressful life events have been linked to declining health, and inflammation has been proposed as a physiological mechanism that might explain this association. Using 828 participants from the Dunedin Longitudinal Study, we tested whether people who experienced more stressful life events during adulthood would show elevated systemic inflammation when followed up in midlife, at age 45. We studied three inflammatory biomarkers: C-reactive protein (CRP), interleukin-6 (IL-6), and a newer biomarker, soluble urokinase plasminogen activator receptor (suPAR), which is thought to index systemic chronic inflammation. Stressful life events were not associated with CRP or IL-6. However, people who experienced more stressful life events from age 38 to 44 had elevated suPAR at age 45, and had significantly greater increases in suPAR from baseline to follow-up across the same period. When examining stressful life events across the lifespan, both adverse childhood experiences (ACEs) and adult stressful life events were independently associated with suPAR at age 45. ACEs moderated the association of adult stressful life events and suPAR at age 45—children with more ACEs showed higher suPAR levels after experiencing stressful life events as adults. The results suggest systemic chronic inflammation is one physiological mechanism that could link stressful life events and health, and support the use of suPAR as a useful biomarker for such research.

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