Nociceptors Are Interleukin-1β Sensors
Harvard University · Massachusetts General Hospital · +3 more institutions
Abstract
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…
Citation impact
- FWCI
- 11.73
- Percentile
- 100%
- References
- 54
Authors
11- AMAlexander M. Binshtok
Harvard University, Massachusetts General Hospital
- HWHaibin Wang
Harvard University, Massachusetts General Hospital
- KZKatharina Zimmermann
Howard Hughes Medical Institute, Harvard University
- FAFumimasa Amaya
Harvard University, Massachusetts General Hospital
- DVDaniel Vardeh
Harvard University, Massachusetts General Hospital
Topics & keywords
- Nociceptor
- Sensitization
- Inflammation
- Hyperalgesia
- Neuroscience
- Proinflammatory cytokine
- p38 mitogen-activated protein kinases
- Medicine
- Good health and well-being