Cited by 107Neuroinflammation and Neurodegeneration MechanismsStress Responses and CortisolNeuropeptides and Animal Physiology

Unraveling the molecular details involved in the intimate link between the immune and neuroendocrine systems

Turrin, Nicolas P., Rivest, Serge·2004·Experimental Biology and Medicine

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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Crossref · 10.1177/153537020422901003

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  • Multiple non-exclusive pathways activate the HPA axis upon cerebral or peripheral immune challenges, including local inflammatory mediators, circulating factors accessing the PVN via circumventricular organs or a disrupted blood-brain barrier, endothelial signaling, and vagus nerve afferents.

    “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.”

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Authors
Turrin, N. P., & Rivest, S.
Affiliations
Centre hospitalier de l'Université Laval (CA)
Corresponding author
Rivest, Serge
Venue
Experimental Biology and Medicine
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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