Psychological stress in adolescent and adult mice increases neuroinflammation and attenuates the response to LPS challenge
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BACKGROUND: There is ample evidence that psychological stress adversely affects many diseases. Recent evidence has shown that intense stressors can increase inflammation within the brain, a known mediator of many diseases. However, long-term outcomes of chronic psychological stressors that elicit a neuroinflammatory response remain unknown. METHODS: To address this, we have modified previously described models of rat/mouse predatory stress (PS) to increase the intensity of the interaction. We postulated that these modifications would enhance the predator-prey experience and increase neuroinflammation and behavioral dysfunction in prey animals. In addition, another group of mice were subjected to a modified version of chronic unpredictable stress (CUS), an often-used model of chronic stress that utilizes a combination of stressors that include physical, psychological, chemical, and other. The CUS model has been shown to exacerbate a number of inflammatory-related diseases via an unknown mechanism. Using these two models we sought to determine: 1) whether chronic PS or CUS modulated the inflammatory response as a proposed mechanism by which behavioral deficits might be mediated, and 2) whether chronic exposure to a pure psychological stressor (PS) leads to deficits similar to those produced by a CUS model containing psychological and physical stressors. Finally, to determine whether acute PS has neuroinflammatory consequences, adult mice were examined at various time-points after PS for changes in inflammation. RESULTS: Adolescent mice subjected to chronic PS had increased basal expression of inflammation within the midbrain. CUS and chronic PS mice also had an impaired inflammatory response to a subsequent lipopolysaccharide challenge and PS mice displayed increased anxiety- and depressive-like behaviors following chronic stress. Finally, adult mice subjected to acute predatory stress had increased gene expression of inflammatory factors. CONCLUSION: Our results demonstrate that predatory stress, an ethologically relevant stressor, can elicit changes in neuroinflammation and behavior. The predatory stress model may be useful in elucidating mechanisms by which psychological stress modulates diseases with an inflammatory component.
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Both physical and psychogenic stressors can abate LPS-induced neuroinflammation as long as they occur after the immune challenge.
“In another study, both physical and psychogenic stressors could abate LPS-induced neuroinflammation, as long as they occurred after the immune challenge (157).”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [157]
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- Authors
- Barnum, C. J., Pace, T. W., Hu, F., Neigh, G. N., & Tansey, M. G.
- Affiliations
- Emory University (US)
- Corresponding author
- Barnum, Christopher J
- Pace, Thaddeus WW
- Hu, Fang
- Neigh, Gretchen N
- Tansey, Malú G
- Venue
- Journal of Neuroinflammation
- Published
- 2012-01-16
- Volume
- 9
- Issue
- 1
- Pages
- 9-9
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC3283491
- OpenAlex
- W2121168584
- Cited by
- 107
- References
- 55
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 6 · 2023: 5 · 2022: 8 · 2021: 6 · 2020: 9 · 2019: 12 · 2018: 10 · 2017: 7 · 2016: 7 · 2015: 7 · 2014: 8 · 2013: 10 · 2012: 1
- FWCI
- 3.45
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health
- National Institute of Mental Health (R21MH085210, 5R21MH85210)
- National Institute of Neurological Disorders and Stroke (R01NS049433, T32NS007480)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- psychological stress, neuroinflammation, chronic unpredictable mild stress, lipopolysaccharide challenge, anxiety-like behavior, depression-like behavior, adolescent mice, inflammatory gene expression, behavioral dysfunction
- MeSH terms
- Aging, Analysis of Variance, Animals, Brain, Corticosterone, Disease Models, Animal, Encephalitis, Food Preferences, Gene Expression Regulation, Male, Mice, Inbred C57BL, Polysaccharides, RNA, Messenger, Stress, Psychological, Sucrose, Sweetening Agents, Cytokines, Hindlimb Suspension, Mice, Rats
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