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The pivotal role of tumour necrosis factor α in the development of inflammatory hyperalgesia
Author(s) -
Cunha F.Q.,
Poole S.,
Lorenzetti B.B.,
Ferreira S.H.
Publication year - 1992
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1992.tb14503.x
Subject(s) - hyperalgesia , tumor necrosis factor alpha , endogeny , medicine , cytokine , beta (programming language) , inflammation , prostaglandin e2 , pharmacology , interleukin , alpha (finance) , prostaglandin e , immunology , endocrinology , nociception , receptor , surgery , construct validity , computer science , patient satisfaction , programming language
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.