The DOI matches its Crossref record; 163 of the 179 references it cites were found in a registry or an index.
Activation of the hypothalamus-pituitary-adrenal axis by bacterial endotoxins: Routes and intermediate signals
Abstract
Peripheral administration of endotoxin induces brain-mediated responses, including activation of the hypothalamus-pituitary-adrenal (HPA) axis and changes in thermoregulation. This paper reviews the mechanisms by which endotoxin affects these responses. The effects on thermoregulation are complex and include macrophage-dependent hyperthermic and hypothermic responses. Low doses of endotoxin, given IP, activate peripheral macrophages to produce interleukin (IL)-1 beta, which enters the circulation and acts as a hormonal signal. IL-1 may pass fenestrated endothelium in the median eminence to stimulate corticotropin-releasing hormone (CRH) secretion from the CRH nerve-terminals. In addition, IL-1 may activate brain endothelial cells to produce IL-1, IL-6, prostaglandins, etc., and secrete these substances into the brain. By paracrine actions, these substances may affect neurons (e.g., CRH neurons) or act on microglial cells, which show IL-1-induced IL-1 production and therefore amplify and prolong the intracerebral IL-1 signal. In contrast, high doses of endotoxin given i.v. may directly stimulate endothelial cells to produce IL-1, IL-6, and prostaglandin-E2 (PGE2) and thereby activate the HPA axis in a macrophage-independent manner.
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“Finally, although circulating LPS does not pass the blood–brain barrier to impact on neurons or glial cells per se [59], LPS modulates the blood–brain barrier function by its direct effect on the tight junction proteins and thus barrier permeability, as well as its interactions with the brain endothelial cells to regulate immune cell trafficking and cytokine transport as an indirect way for gut”
In the citing paper
“By binding to its receptors on macrophages, lymphocytes, and granulocytes, LPS induces cytokine production (notably interleukin-1, interleukin-6 and tumor necrosis factor-α) from immune cells and triggers a series of changes in the immune-endocrine-nervous system that subsequently activates the HPA axis (for details please refer to a comprehensive review by Tilders and colleagues [59]).”
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1 retracted
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The Hypothalamic–Pituitary–Adrenal Axis and Immune-Mediated Inflammation
Chrousos, G. P. (1995) · New England Journal of Medicine · doi:10.1056/nejm199505183322008 · Cited by 2,579
Cytokine Pathways and Joint Inflammation in Rheumatoid Arthritis
Choy, E., & Panayi, G. S. (2001) · New England Journal of Medicine · doi:10.1056/nejm200103223441207 · Cited by 2,248
Regulation of the Hypothalamic-Pituitary-Adrenal Axis by Cytokines: Actions and Mechanisms of Action
TURNBULL, A. V., & RIVIER, C. L. (1999) · Physiological Reviews · doi:10.1152/physrev.1999.79.1.1 · Cited by 1,297
Tomiyama, A. J. (2019) · Annual Review of Psychology · doi:10.1146/annurev-psych-010418-102936 · Cited by 695
“F or p er so na l u se o nl y. too heavy a body (Tomiyama 2014), weight stigma is pervasive.”
BackgroundResultInfluentialDepression, stress and immunological activation: The role of cytokines in depressive disorders
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Metadata
- Authors
- Tilders, F. J. H., DeRuk, R. H., Van Dam, A.-M., Vincent, V. A. M., Schotanus, K., & Persoons, J. H. A.
- Affiliations
- Vrije Universiteit Amsterdam (NL)
- Corresponding author
- Tilders, Fred J.H.
- Venue
- Psychoneuroendocrinology
- Publisher
- Elsevier BV
- Published
- 1994
- Volume
- 19
- Issue
- 2
- Pages
- 209-232
- ISSN
- 0306-4530 (ISSN-L)
- OpenAlex
- W1989306597
- Cited by
- 277
- References
- 179
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 2 · 2019: 1 · 2018: 4 · 2017: 1 · 2016: 2 · 2015: 2 · 2014: 5 · 2013: 5 · 2012: 2
- FWCI
- 3.73
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Psychoneuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Thermal Regulation in Medicine
- Keywords
- hypothalamic-pituitary-adrenal axis, bacterial endotoxin, IL-1β, thermoregulation, corticotropin-releasing factor, median eminence, brain endothelial cells, microglia, prostaglandin E2, interleukin-6, macrophages, neuroendocrine signaling
- MeSH terms
- Adrenocorticotropic Hormone, Afferent Pathways, Animals, Corticosterone, Endothelium, Vascular, Endotoxins, General Adaptation Syndrome, Hypothalamo-Hypophyseal System, Interleukin-1, Macrophage Activation, Pituitary-Adrenal System, Dinoprostone, Signal Transduction, Interleukin-6
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