Stress-induced release of the S100A8/A9 alarmin is elevated in coronary artery disease patients with impaired cortisol response
(2017) In Scientific Reports 7(1).- 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... (More)
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.
(Less)
- author
- Jonasson, L.
; Larsen, H. Grauen
LU
; Lundberg, A. K.
; Gullstrand, B.
LU
; Bengtsson, A. A.
LU
and Schiopu, A.
LU
- organization
- publishing date
- 2017-12-01
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Scientific Reports
- volume
- 7
- issue
- 1
- article number
- 17545
- publisher
- Nature Publishing Group
- external identifiers
-
- scopus:85038420972
- pmid:29235502
- wos:000417796000065
- ISSN
- 2045-2322
- DOI
- 10.1038/s41598-017-17586-6
- language
- English
- LU publication?
- yes
- id
- cbda45c7-18c4-4087-bf2a-0faa17d914e9
- date added to LUP
- 2018-01-03 14:27:44
- date last changed
- 2025-01-08 01:39:49
@article{cbda45c7-18c4-4087-bf2a-0faa17d914e9, abstract = {{<p>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.</p>}}, author = {{Jonasson, L. and Larsen, H. Grauen and Lundberg, A. K. and Gullstrand, B. and Bengtsson, A. A. and Schiopu, A.}}, issn = {{2045-2322}}, language = {{eng}}, month = {{12}}, number = {{1}}, publisher = {{Nature Publishing Group}}, series = {{Scientific Reports}}, title = {{Stress-induced release of the S100A8/A9 alarmin is elevated in coronary artery disease patients with impaired cortisol response}}, url = {{http://dx.doi.org/10.1038/s41598-017-17586-6}}, doi = {{10.1038/s41598-017-17586-6}}, volume = {{7}}, year = {{2017}}, }