PGE2 released by primary sensory neurons modulates Toll-like receptor 4 activities through an EP4 receptor-dependent process

Kai Hei Tse, Kevin B.S. Chow, Helen Wise

Research output: Journal article publicationJournal articleAcademic researchpeer-review

2 Citations (Scopus)


Exogenous prostaglandin E2 (PGE2) displays mixed regulatory properties with regard to inflammatory gene expression in dorsal root ganglion (DRG) cells. We show here that endogenously-produced nanomolar concentrations of PGE2, such as that generated in response to Toll-like receptor 4 (TLR4) stimulation, inhibits both cyclooxygenase-2 (COX-2) and tumour necrosis factor alpha (TNFα) mRNA expression in DRG cells in an EP4 receptor-dependent manner. DRG neurons appear to be the major source of PGE2 in the DRG and likely serve as both an autocrine and paracrine system for limiting over-activation of both DRG neurons and glial cells in response to TLR4 stimulation.

Original languageEnglish
Pages (from-to)8-16
Number of pages9
JournalJournal of Neuroimmunology
Early online date10 Feb 2016
Publication statusPublished - 15 Apr 2016
Externally publishedYes


  • Dorsal root ganglia
  • EP
  • PGE
  • Primary sensory neurons
  • Toll-like receptor 4

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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