Nociceptors are interleukin-1beta sensors.

Journal Article (Journal Article)

A cardinal feature of inflammation is heightened pain sensitivity at the site of the inflamed tissue. This results from the local release by immune and injured cells of nociceptor sensitizers, including prostaglandin E(2), bradykinin, and nerve growth factor, that reduce the threshold and increase the excitability of the peripheral terminals of nociceptors so that they now respond to innocuous stimuli: the phenomenon of peripheral sensitization. We show here that the proinflammatory cytokine interleukin-1beta (IL-1beta), in addition to producing inflammation and inducing synthesis of several nociceptor sensitizers, also rapidly and directly activates nociceptors to generate action potentials and induce pain hypersensitivity. IL-1beta acts in a p38 mitogen-activated protein kinase (p38 MAP kinase)-dependent manner, to increase the excitability of nociceptors by relieving resting slow inactivation of tetrodotoxin-resistant voltage-gated sodium channels and also enhances persistent TTX-resistant current near threshold. By acting as an IL-1beta sensor, nociceptors can directly signal the presence of ongoing tissue inflammation.

Full Text

Duke Authors

Cited Authors

  • Binshtok, AM; Wang, H; Zimmermann, K; Amaya, F; Vardeh, D; Shi, L; Brenner, GJ; Ji, R-R; Bean, BP; Woolf, CJ; Samad, TA

Published Date

  • December 24, 2008

Published In

Volume / Issue

  • 28 / 52

Start / End Page

  • 14062 - 14073

PubMed ID

  • 19109489

Pubmed Central ID

  • PMC2690713

Electronic International Standard Serial Number (EISSN)

  • 1529-2401

Digital Object Identifier (DOI)

  • 10.1523/JNEUROSCI.3795-08.2008


  • eng

Conference Location

  • United States