The pivotal role of tumour necrosis factor α in the development of inflammatory hyperalgesia
Abstract
- 1
The hyperalgesic activities in rats of interleukin-1β (IL-1β), IL-6, IL-8, tumour necrosis factor α (TNFα) and carrageenin were investigated.
- 2
IL-6 activated the previously delineated IL-1/prostaglandin hyperalgesic pathway but not the IL-8/sympathetic mediated hyperalgesic pathway.
- 3
TNFα and carrageenin activated both pathways.
- 4
Antiserum neutralizing endogenous TNFα abolished the response to carrageenin whereas antisera neutralizing endogenous IL-1β, IL-6 and IL-8 each partially inhibited the response.
- 5
The combination of antisera neutralizing endogenous IL-1β + IL-8 or IL-6 + IL-8 abolished the response to carrageenin.
- 6
These results show that TNFα has an early and crucial role in the development of inflammatory hyperaglesia.
- 7
The delineation of the roles of TNFα, IL-1β, IL-6 and IL-8 in the development of inflammatory hyperalgesia taken together with the finding that the production of these cytokines is inhibited by steroidal anti-inflammatory drugs provides a mechanism of action for these drugs in the treatment of inflammatory hyperalgesia.