ICU sedation, delirium & recovery
Cell-specific expression and signaling of glucocorticoid receptor isoforms over time in critically ill patients with a low inflammatory response
Authors' conclusion
PMNs show reduced GCR-α/β/γ with preserved GILZ, while PBMCs maintain GCR-α/β/γ but upregulate GCR-P and DUSP1.
Study context
- Population
- Critically ill patients with a low inflammatory response; blood sampled at ICU admission (24–48 h) and days 4, 8 and 14
- Exposure
- Critically ill patients vs healthy controls
- Outcome
- mRNA expression of GCR variants (GCR-α, GCR-β, GCR-γ, GCR-P) and glucocorticoid (GC) downstream targets (GILZ, DUSP1) in PMNs and PBMCs (RT-PCR)
- Follow-up
- ICU admission (24-48 h) and days 4, 8 and 14
Methodological detailslongitudinal
- Longitudinal
Main finding
As reported in the abstract
GCR isoform and downstream target expression vs controls
- PMNs: sustained downregulation of glucocorticoid receptor (GCR)-α, GCR-β and GCR-γ, with preserved GC-induced leucine zipper (GILZ) expression; GCR-P stable
- Peripheral blood mononuclear cells (PBMCs): GCR-α, GCR-β, GCR-γ and GILZ no significant changes vs controls; GCR-P upregulated
- DUSP1 downregulated in PMNs and elevated in PBMCs
Observational data: associations, not effects.
Further findings
Correlation of IL-6 with GILZ and DUSP1
- Negative correlations between IL-6 and both GILZ and DUSP1
Expression patterns over time · 2 weeks
- All expression patterns stable across time points despite dynamic adrenocorticotropic hormone (ACTH) changes and persistently elevated cortisol
- Subset of patients who completed the 2-week study
Parts of this Brief are withheld: the automatic checks could not confirm them against the abstract.
Original publication
Cell-specific expression and signaling of glucocorticoid receptor isoforms over time in critically ill patients with a low inflammatory response. Crit Care. Published 29 August 2025. doi:10.
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