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Single-cell transcriptomics provides insights into the stress-immune interplay and informs disease risk

ABSTRACT: Environmental stress contributes to many disease conditions – including cardiovascular disease, mental illness, and autoimmune disorders – through immune dysregulation. Stress operates through the hypothalamic-pituitary-adrenal and sympathoadrenal axes, leading to peripheral secretion of cortisol and norepinephrine, respectively. While stress hormones can profoundly influence immune function, their mechanistic effects at the cell-type level remain poorly understood. To address this knowledge gap, we employed an ex vivo model investigating the transcriptomic responses of primary peripheral blood mononuclear cells and neutrophils to physiological stress levels (i.e., levels reached during in vivo stress) of cortisol and norepinephrine at single-cell resolution. We identified novel stress-hormone-dependent and cell-type-specific transcriptomic changes, including uniquely regulated genes and inflammation-related signatures within distinct innate (e.g., CD163+ monocytes/macrophages, neutrophils) and other immune cell types. The single-cell-derived signatures effectively distinguished individuals with stress-related diseases in two independent human cohorts. Our findings provide cell-type-level insights into how stress hormones modulate immune function relevant to stress-related conditions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE334840 | GEO | 2026/07/17

REPOSITORIES: GEO

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Project description:The ability to respond to stress is at the core of an organismâs survival. The hormones epinephrine and norepinephrine play a central role in stress responses in mammals, which require the synchronized interaction of the whole neuroendocrine system. Bacteria also sense and respond to epinephrine and norepinephrine as a means to gauge the metabolic and immune state of the host. Mammalian adrenergic receptors are G-coupled protein receptors (GPCRs), bacteria, however, sense these hormones through histidine sensor kinases (HKs). HKs autophosphorylate in response to multiple signals and transfer this phosphate to response regulators (RRs). Two bacterial adrenergic receptors have been identified in EHEC, QseC and QseE, with QseE being downstream of QseC in this signaling cascade. We mapped the QseC signaling cascade in the deadly pathogen enterohemorrhagic E. coli (EHEC), which exploits this signaling system to promote disease. Through QseC, EHEC activates expression of metabolic, virulence and stress response genes, synchronizing the cell response to these stress hormones. Coordination of these responses is achieved by QseC phosphorylating three of the thirty two EHEC RRs. The QseB RR, which is QseCâs cognate RR, activates the flagella regulon which controls bacteria motility and chemotaxis. The QseF RR, which is phosphorylated by the QseE adrenergic sensor, coordinates expression of virulence genes involved in formation of lesions in the intestinal epithelia by EHEC, and the bacterial SOS stress response. The third RR, KdpE, controls potassium uptake, osmolarity response, and also the formation of lesions in the intestine. Adrenergic regulation of bacterial gene expression shares several parallels with mammalian adrenergic signaling having profound effects in the whole organism. Understanding adrenergic regulation of a bacterial cell is a powerful approach to study the underlying mechanisms of stress and cellular survival. Experiment Overall Design: Microarray comparisons reveal some trends with respect to signaling cascades. Comparative methods were used to identify networks.

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Single-cell transcriptomics provides insights into the stress-immune interplay and informs disease risk

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