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Sci Rep. 2017 Dec 13;7(1):17545. doi: 10.1038/s41598-017-17586-6.

Stress-induced release of the S100A8/A9 alarmin is elevated in coronary artery disease patients with impaired cortisol response.

Author information

1
Division of Cardiovascular Medicine, Department of Medical and Health Sciences, Linköping University, Linköping, Sweden.
2
Experimental Cardiovascular Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
3
Department of Cardiology, Skane University Hospital Malmö, Malmö, Sweden.
4
Section of Rheumatology, Department of Clinical Sciences Lund, Lund University and Skane University Hospital Lund, Lund, Sweden.
5
Experimental Cardiovascular Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden. Alexandru.Schiopu@med.lu.se.
6
Department of Cardiology, Skane University Hospital Malmö, Malmö, Sweden. Alexandru.Schiopu@med.lu.se.

Abstract

Psychological stress is thought to be an important trigger of cardiovascular events, yet the involved pathways and mediators are largely unknown. Elevated systemic levels of the pro-inflammatory alarmin S100A8/A9 correlate with poor prognosis in coronary artery disease (CAD) patients. Here, we investigated the links between S100A8/A9 release and parameters of anti-inflammatory glucocorticoid secretion in two different cohorts subjected to a psychological stress test. In the first cohort of 60 CAD patients, psychological stress induced a rapid increase of circulating S100A8/A9. This rapid S100A8/A9 response strongly correlated with elevated evening saliva cortisol levels, suggesting an association with a dysregulated hypothalamic-pituitary-adrenal (HPA) axis. In the second cohort of 27 CAD patients and 28 controls, elevated S100A8/A9 levels were still detectable 24 h after stress in 40% of patients and 36% of controls, with a tendency for higher levels in patients. The sustained S100A8/A9 response was associated with a poor rapid cortisol release after stress in patients, but not in the control group. Our findings reveal for the first time that acute psychological stress induces elevated levels of S100A8/A9. We also provide hypothesis-generating evidence that dysregulated cortisol secretion in CAD patients might be associated with an exaggerated pro-inflammatory S100A8/A9 response.

PMID:
29235502
PMCID:
PMC5727540
DOI:
10.1038/s41598-017-17586-6
[Indexed for MEDLINE]
Free PMC Article

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