• J. Neuroimmunol. · Apr 2016

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

    • Kai-Hei Tse, Chow Kevin B S KBS School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China., and Helen Wise.
    • School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China. Electronic address: frankitse@ust.hk.
    • J. Neuroimmunol. 2016 Apr 15; 293: 8-16.

    AbstractExogenous 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. Copyright © 2016 Elsevier B.V. All rights reserved.

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