Interleukin-1β as a potent hyperalgesic agent antagonized by a tripeptide analogue

@article{Ferreira1988Interleukin1AA,
  title={Interleukin-1$\beta$ as a potent hyperalgesic agent antagonized by a tripeptide analogue},
  author={S{\'e}rgio H. Ferreira and Berenice B. Lorenzetti and Adrian F. Bristow and Stephen Poole},
  journal={Nature},
  year={1988},
  volume={334},
  pages={698-700}
}
Interleukin-1 (IL-1) describes two inflammatory proteins1, IL-1α and IL-1β, produced by activated macrophages and other cell types2 and encoded by two genes. Their amino acid sequences have only 26% similarity1, but their biological activities are comparable, with a few exceptions3,4; indeed, both molecules appear to act at the same receptor5,6. As IL-1 releases prostaglandins7 which sensitize nociceptors in man and in experimental animals8, we tested IL-1α and IL-1β in rats for hyperalgesic… 
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599 Citations

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Blockade of inflammatory hyperalgesia and cyclooxygenase-2
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Using specific antisera and COX inhibitors it is demonstrated that interleukin-lβ (IL-1β) is a key cytokine for the release of prostaglandins (PG) and induction of COX-2 is a limiting process in the development of inflammatory hyperalgesia.
IL-33 mediates antigen-induced cutaneous and articular hypernociception in mice
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It is demonstrated that methylated BSA (mBSA) induced hypernociception via the IL-33 → TNFα → IL-1β → IFNγ → ET-1 → PGE2 signaling cascade, revealing a hitherto unrecognized function of IL- 33 in a key immune pharmacological pathway that may be amenable to therapeutic intervention.
Inhibition by neuropeptides of interleukin‐1β‐induced, prostaglandin‐independent hyperalgesia
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Observations indicate that IL‐1β sensitized pressure‐sensitive but not temperature‐sensitive sensory neurones, through a prostaglandin‐independent mechanism.
Confluence of antianalgesic action of diverse agents through brain interleukin(1beta) in mice.
  • J. Rady, J. Fujimoto
  • Biology, Medicine
    The Journal of pharmacology and experimental therapeutics
  • 2001
TLDR
IL1beta is a central physiological mediator in the antianalgesic action evoked by spinal dynorphin as shown by inhibition with appropriate antagonists.
Role of Thymulin or Its Analogue as a New Analgesic Molecule
TLDR
Preliminary results demonstrate that thymulin inhibits in the hippocampus the ET‐induced nuclear activation of NF‐κB, the transcription factor required for the expression of proinflammatory cytokines genes.
IL-15 mediates immune inflammatory hypernociception by triggering a sequential release of IFN-gamma, endothelin, and prostaglandin.
  • W. Verri, T. Cunha, F. Cunha
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 2006
TLDR
The results demonstrate the sequential mechanical hypernociceptive effect of IL-15 --> IFN-gamma --> ET-1 --> PGE(2) and suggest that these molecules may be targets of therapeutic intervention in antigen-induced hyperNociception.
Effects of nonsteroidal anti-inflammatory drugs on interleukin-1 receptor antagonist production in cultured human peripheral blood mononuclear cells.
Interleukin-1 and interleukin-1 fragments as vaccine adjuvants.
TLDR
Human interleukin-1beta domain in position 163-171, comprising the amino acids VQGEESNDK, has been synthesized as a nine-amino-acid-long peptide and used in vivo as a nontoxic HCl salt, and the DNA sequence encoding the IL-1 beta domain has been included in an experimental DNA vaccine with positive results.
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It is shown here that the receptor for IL-1α on both murine and human cells is identical to that forIL-1β, which raises the issue of what separation, if any, there might be between the biological activities of IL- 1α and IL-2β.
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