Acute and chronic stress induced changes in sensitivity of peripheral inflammatory pathways to the signals of multiple stress systems – 2011 Curt Richter Award Winner
Abstract
Exposure to psychosocial stress has been associated with increasing rates of morbidity in humans and in animal models, but the underlying mechanisms are not completely understood. Major stress responsive systems, such as the hypothalamus-pituitary adrenal (HPA) axis and the autonomic nervous system (ANS) are under investigation as underlying pathways, but although acute stress reliably activates these systems, findings of long-term alternations in baseline activity are inconsistent at present. Emerging evidence suggests that stress-related changes in the sensitivity of target systems toward glucocorticoid (GC) regulation, i.e. development of GC resistance, might help explain inflammatory disinhibition and development of disease related to inflammation. More recent findings further show that the autonomic nervous system might play an important role in the regulatory control of the inflammatory cascade. The major argument put forward in this manuscript is that target tissues for stress system modulation, such as the inflammatory cascade, vary in their ability to respond to stress system signaling, and that assessing alterations in this stress signal sensitivity which can be caused by stress or disease processes, might be necessary to understand and explain stress effects on health. This review focuses on the inflammatory system in particular, because anti-inflammatory effects of most stress systems have been documented, but the general assumption might have to be generalized to other target systems. The main conclusion to be made is that reduction in glucocorticoid sensitivity of target tissues is the most consistent finding at present, and that assessing such changes in glucocorticoid sensitivity might be necessary to understand many stress-related changes in physiology.
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Peripheral inhibition of IL-1 by the IL-1ra anakinra over a 4-week period did not lead to clinically significant reduced fatigue in women with ME/CFS compared with a placebo group.
“peripheral inhibition of IL-1 by the IL-1ra anakinra over a 4-wk period did not lead to clinically significant reduced fatigue in women with ME/CSF compared with a placebo group (473).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [473]
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Social Stress Mobilizes Hematopoietic Stem Cells to Establish Persistent Splenic Myelopoiesis
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- Authors
- Rohleder, N.
- Affiliations
- Brandeis University (US)
- Corresponding author
- Rohleder, Nicolas
- ORCID
- Rohleder, Nicolas
- Venue
- Psychoneuroendocrinology
- Publisher
- Elsevier BV
- Published
- 2012-03
- Volume
- 37
- Issue
- 3
- Pages
- 307-316
- ISSN
- 0306-4530 (ISSN-L)
- OpenAlex
- W2143364563
- Cited by
- 136
- References
- 96
- Citations by year
- 2026: 2 · 2025: 11 · 2024: 6 · 2023: 3 · 2022: 10 · 2021: 13 · 2020: 9 · 2019: 10 · 2018: 10 · 2017: 9 · 2016: 13 · 2015: 13 · 2014: 10 · 2013: 7 · 2012: 9
- FWCI
- 0.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Psychoneuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- German Research Foundation (DFG)
- Michael Smith Foundation for Health Research
- American Federation for Aging Research
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- psychosocial stress, acute stress, chronic stress, hypothalamic-pituitary-adrenal axis, autonomic nervous system, glucocorticoid resistance, glucocorticoid sensitivity, inflammatory cascade, inflammation, stress-related disorders
- MeSH terms
- Animals, Autonomic Nervous System, Glucocorticoids, Humans, Hypothalamo-Hypophyseal System, Inflammation, Pituitary-Adrenal System, Stress, Psychological, Signal Transduction, Inflammation Mediators
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