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EV0648

Temporal dynamics of whole-blood transcriptional responses to acute psychosocial stress

TEMPORAL DYNAMICS OF WHOLE-BLOOD TRANSCRIPTIONAL RESPONSES TO ACUTE PSYCHOSOCIAL STRESS

Acute psychosocial stress induces a broad and sustained transcriptomic response in whole blood, which separates into three distinct temporal patterns: acute cytotoxic, delayed innate immune, and translation-related responses.

The study aimed to characterize the temporal dynamics of gene expression changes following acute stress in humans using whole-blood stress transcriptomics. A total of 306 participants underwent the Trier Social Stress Test (TSST); blood samples were collected before the test and at 30-minute intervals for up to 90 minutes afterward while participants rested. Whole-blood gene expression was analyzed using spline-based time models, followed by trajectory clustering to identify distinct patterns of change and enrichment analyses to characterize functional pathways. Of the 24,268 genes tested, 15,205 showed a significant time-course effect (false discovery rate, FDR <0.05); data-driven clustering identified three clusters with moderate silhouette (0.519) and stability (0.527) values. Cluster 1 (n=5019) represents a broad translation- and ribosome-related program and showed a slight increase at 30 minutes followed by a decline during late recovery; representative genes include RPL22, RPS4X, RPL7P9, and NPM1. Cluster 2 (n=6489) was downregulated immediately after the TSST and increased during recovery, and was associated with neutrophil granules, heme metabolism, and innate immune activation (S100A8, S100A12, ST3GAL6, TLR2, C5AR1); Cluster 3 (n=3697) increased after the TSST and declined during recovery, and was associated with natural killer cell and cytotoxic lymphocyte programs (GNLY, GZMB, SH2D1B, B3GAT1, PRF1). Sensitivity analyses showed that blood cell composition accounted for a substantial portion of the response (8092 genes after controlling for the first two principal components, FDR <0.05) and that the cortisol response modified the expression trajectories of a subset of genes (3356 genes for the cortisol-by-time interaction term, FDR <0.05). The authors note that the response cannot be reduced to a simple pattern of post-stress activation followed by a decline during recovery, and that these divergent trajectories warrant further investigation.

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