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Unraveling the Molecular Details Involved in the Intimate Link between the Immune and Neuroendocrine Systems
Abstract
During systemic infections, the immune system can signal the brain and act on different neuronal circuits via soluble molecules, such as proinflammatory cytokines, that act on the cells forming the blood-brain barrier and the circumventricular organs. These activated cells release prostaglandin of the E(2) type (PGE(2)), which is the endogenous ligand that triggers the pathways involved in the control of autonomic functions necessary to restore homeostasis and provide inhibitory feedback to innate immunity. Among these neurophysiological functions, activation of the circuits that control the plasma release of glucocorticoids is probably the most critical to the survival of the host in the presence of pathogens. This review revisits this issue and describes in depth the molecular details (including the emerging role of Toll-like receptors during inflammation) underlying the influence of circulating inflammatory molecules on the cerebral tissue, focusing on their contribution in the synthesis and action PGE(2) in the brain. We also provide an innovative view supporting the concept of "fast and delayed response" involving the same ligands but different groups of cells, signal transduction pathways, and target genes.
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“Multiple non-exclusive pathways participate in the activation of the HPA axis upon cerebral or peripheral immune challenges. When an immunogenic insult takes place in the brain, various inflammatory mediators produced locally may trigger the HPA axis.”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [15]
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Background
Metadata
- Authors
- Turrin, N. P., & Rivest, S.
- Affiliations
- Centre hospitalier de l'Université Laval (CA)
- Corresponding author
- Rivest, Serge
- ORCID
- Rivest, Serge
- Venue
- Experimental Biology and Medicine
- Publisher
- Frontiers Media SA
- Published
- 2004-11
- Volume
- 229
- Issue
- 10
- Pages
- 996-1006
- ISSN
- 0071-3384 (ISSN-L)
- 1535-3702
- 1535-3699
- OpenAlex
- W1760516212
- Cited by
- 107
- References
- 99
- Citations by year
- 2026: 1 · 2024: 6 · 2023: 2 · 2022: 4 · 2021: 3 · 2020: 1 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 6 · 2015: 3 · 2014: 6 · 2013: 7 · 2012: 7
- FWCI
- 0.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- neuroimmune interactions, neuroendocrine system, inflammatory cytokines, prostaglandin E2, blood-brain barrier, circumventricular organs, hypothalamic-pituitary-adrenal axis, Toll-like receptors, systemic infection, inflammation, signal transduction
- MeSH terms
- Animals, Autonomic Nervous System, Blood-Brain Barrier, Glucocorticoids, Humans, Hypothalamo-Hypophyseal System, Immune System, Molecular Biology, Neurosecretory Systems, Receptors, Cell Surface, Dinoprostone, Signal Transduction, Cytokines, Inflammation Mediators
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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