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Cited by 439Stress Responses and CortisolCancer, Stress, Anesthesia, and Immune ResponseTryptophan and brain disorders

Stress and inflammation – The need to address the gap in the transition between acute and chronic stress effects

Rohleder, Nicolas·2019·Psychoneuroendocrinology
DOI 10.1016/j.psyneuen.2019.02.021
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Abstract

Stress responses help us navigate our environment and respond appropriately to threats. Stress systems communicate threats to the entire organism, and as such, also stimulate inflammatory mechanisms. This modulation might serve protective functions in the short term, but sustained low-grade inflammation has severe long-term health consequences. While we have reached a reasonable level of understanding of acute, as well as chronic stress effects on inflammatory mechanisms, there is a significant gap in our understanding of the transitional phase between acute and chronic stress. The purpose of this review is to first summarize current knowledge of our understanding of acute stress effects on inflammation, as well as of chronic stress effects on inflammation, and to then analyze the state of knowledge about the transitional phase between acute and chronic stress. Research discussed here shows that we are beginning to understand the early phase of repeated acute stress, but lack information on longer term exposure to repeated acute stress experiences. More research is needed to bridge this important gap und our conceptualization and understanding of the stress and health relationship.

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Crossref · 10.1016/j.psyneuen.2019.02.021

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  • Glucocorticoid desensitization dampens the immune system's response to cortisol, leading to elevated peripheral pro-inflammatory factors (TNF, IL-17, IL-1β, IL-6) and sustained neuroinflammation marked by chronic microglial and astrocyte activation.

    “This desensitization dampens the immune system’s response to cortisol, ultimately leading to elevated peripheral pro-inflammatory factors (e.g., TNF, IL-17, IL-1β, IL-6) and sustained neuroinflammation, marked by chronic microglial and astrocyte activation [29,31,32,33,34].”

    From Comparative Analysis of HPA-Axis Dysregulation and Dynamic Molecular Mechanisms in Acute Versus Chronic Social Defeat Stress (2025) · cites this paper as [29]

  • Chronic stress disrupts key neurotransmitter systems, alters neuronal connectivity, and disturbs synaptic network activity, leading to dysregulated excitatory glutamatergic signaling, impaired dopaminergic transmission, and altered inhibitory GABAergic signaling in specific brain regions.

    “Concurrently, chronic stress disrupts key neurotransmitter systems, alters neuronal connectivity, and disturbs synaptic network activity, leading to, for example, dysregulated excitatory glutamatergic signaling, impaired dopaminergic transmission, and altered inhibitory GABAergic signaling in specific brain regions [4,24,29,35,36,37].”

    From Comparative Analysis of HPA-Axis Dysregulation and Dynamic Molecular Mechanisms in Acute Versus Chronic Social Defeat Stress (2025) · cites this paper as [29]

  • Prolonged or excessive stress can overwhelm homeostatic capacity, leading to sustained overactivation of the HPA axis, which drives chronic low-grade inflammation implicated in psychiatric disorders such as depression and anxiety.

    “While early stress may be adaptively regulated by the body, prolonged or excessive stress can overwhelm the organism’s homeostatic capacity, leading to sustained overactivation of the HPA axis [28]. This drives a state of chronic low-grade inflammation, which has been implicated in the development of various psychiatric disorders, such as depression and anxiety [29].”

    From Comparative Analysis of HPA-Axis Dysregulation and Dynamic Molecular Mechanisms in Acute Versus Chronic Social Defeat Stress (2025) · cites this paper as [29]

  • Collection of heart rate data in laboratory or medical environments lacks temporal resolution within and across days as heart rate is usually collected during a short recording within a single day, which has precluded research from comprehensively investigating the transition from acute to chronic stress.

    “Second, collection of HR data in these environments lacks temporal resolution within and across days as HR is usually collected during a short recording within a single day, which has precluded research from comprehensively investigating the transition from acute to chronic stress22.”

    From Guidelines for wrist-worn consumer wearable assessment of heart rate in biobehavioral research (2020) · cites this paper as [22]

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Authors
Rohleder, N.
Affiliations
Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
Corresponding author
Rohleder, Nicolas
ORCID
Rohleder, Nicolas
Venue
Psychoneuroendocrinology
Publisher
Elsevier BV
Published
2019-07
Volume
105
Pages
164-171
ISSN
0306-4530 (ISSN-L)
DOI
10.1016/j.psyneuen.2019.02.021
OpenAlex
W2915374223
Semantic Scholar
5f2b6ce5b61e4353e8706b16ee5040ca82003395
Cited by
439
References
113
Citations by year
2026: 55 · 2025: 76 · 2024: 64 · 2023: 119 · 2022: 59 · 2021: 39 · 2020: 19 · 2019: 7
FWCI
3.59
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Psychoneuroendocrinology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
acute stress, chronic stress, low-grade inflammation, stress response, inflammatory mechanisms, stress and health
MeSH terms
Acute Disease, Chronic Disease, Habituation, Psychophysiologic, Humans, Hypothalamo-Hypophyseal System, Inflammation, Stress, Psychological

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