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Central serotonin attenuates LPS-induced systemic inflammation.

Clarissa M D Mota1, Caroline Rodrigues-Santos2, Rodrigo A R Fernández1

  • 1Department of Physiology, Medical School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.

Brain, Behavior, and Immunity
|July 21, 2017
PubMed
Summary
This summary is machine-generated.

Central serotonin (5-HT) acts as an anti-inflammatory neuromodulator. This study shows that 5-HT levels decrease during systemic inflammation, and restoring 5-HT can reduce inflammatory responses and fever.

Keywords:
CorticosteroneEndotoxinFeverHeat loss indexIL-6LPSThermoregulation

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Serotonin (5-HT) is a key neuromodulator in the central nervous system, influencing behavior, sleep, and endocrine functions.
  • While 5-HT dysfunction is linked to psychiatric disorders, its role in modulating systemic inflammation (SI) is not well understood.
  • Emerging evidence suggests immune system activation can impact central 5-HT signaling.

Purpose of the Study:

  • To investigate whether central 5-HT modulates lipopolysaccharide (LPS)-induced systemic inflammation in rats.
  • To examine the effects of central 5-HT administration on key inflammatory markers and thermoregulation during SI.
  • To elucidate the relationship between 5-HT signaling in the anteroventral preoptic region (AVPO) and the inflammatory response.

Main Methods:

  • Male Wistar rats were subjected to LPS-induced SI.
  • Levels of 5-HT and its metabolite 5-hydroxyindole-3-acetic acid (5-HIAA) were measured in the AVPO.
  • Body temperature (Tb), AVPO prostaglandin E2 (PGE2) and D2 (PGD2), plasma corticosterone (CORT), and interleukin-6 (IL-6) were assessed.
  • Intracerebroventricular (icv) injections of 5-HT were administered in combination with LPS.

Main Results:

  • LPS induced increased Tb, AVPO PGE2, plasma CORT and IL-6, and decreased heat loss index (HLI), accompanied by reduced AVPO 5-HT and 5-HIAA.
  • A U-shaped dose-response curve was observed for icv 5-HT's effect on LPS-induced fever, with an intermediate dose reducing the febrile response.
  • Central 5-HT administration (10μg/μL) prevented LPS-induced increases in AVPO PGE2, plasma CORT and IL-6, and normalized HLI.

Conclusions:

  • Central 5-HT acts as an anti-inflammatory neuromodulator, counteracting LPS-induced systemic inflammation.
  • Down-regulation of AVPO 5-HT synthesis during SI may potentiate inflammatory responses via increased AVPO PGE2.
  • Modulation of central 5-HT pathways presents a potential therapeutic strategy for inflammatory diseases and could be relevant in treating psychiatric disorders with 5-HT reuptake inhibitors.