Cytokine‐mediated inflammatory hyperalgesia limited by interleukin‐10

  title={Cytokine‐mediated inflammatory hyperalgesia limited by interleukin‐10},
  author={Stephen Poole and Fernando de Q Cunha and Stephen M. Selkirk and Berenice B. Lorenzetti and Sérgio Henrique Ferreira},
  journal={British Journal of Pharmacology},
1 The effect of interleukin‐10 (IL‐10) upon the hyperalgesic activities in rats of bradykinin, tumor necrosis factor α (TNFα), interleukin‐1β (IL‐1β), interleukin‐6 (IL‐6), interleukin‐8 (IL‐8), prostaglandin E2 (PGE2) and carrageenin were investigated in a model of mechanical hyperalgesia. 2 Hyperalgesic responses to bradykinin (1 μg) were inhibited in a dose‐dependent manner by prior treatment with IL‐10 (1–100 ng). 3 Hyperalgesic responses to TNFα (2.5 pg), IL‐1β (0.5 pg) and IL‐6 (1.0 ng… 

Cytokine‐mediated inflammatory hyperalgesia limited by interleukin‐4

The data suggest that IL‐4 released by mast cells limits inflammatory hyperalgesia, and that in the later phase of the response, in addition to inhibiting the production of pro‐inflammatory cytokines, IL‐ 4 also may inhibit the release of PGs.

Anti‐inflammatory and analgesic effects of paeonol in carrageenan‐evoked thermal hyperalgesia

  • T. Chou
  • Medicine, Biology
    British journal of pharmacology
  • 2003
The results suggest that the mechanisms by which paeonol exerts its anti-inflammatory and analgesic effects in this inflammatory model may be associated with decreased production of proinflammatory cytokines, NO and PGE2 and increased production of IL‐10, an anti‐inflammatory cytokine, in carrageenan‐injected rat paws.

Modulation of ultraviolet‐induced hyperalgesia and cytokine upregulation by interleukins 10 and 13

The hyperalgesia and cytokine upregulation induced by UVB and their modulation by antiinflammatory cytokines were characterized to show a biphasic temporal evolution with an acute phase and a late phase, since both were prevented by treatment with anti inflammatory cytokines.

Interleukin‐8 production by the human colon epithelial cell line HT‐29: modulation by interleukin‐13

It is suggested that colonic epithelial cells have a functional IL‐13 receptor, which is coupled to an up‐regulation of IL‐1α, but not TNF‐α induced IL‐8 generation.

Antinociceptive Effects of Interleukin-4, -10, and -13 on the Writhing Response in Mice and Zymosan-Induced Knee Joint Incapacitation in Rats

The results demonstrate that IL-4, -10, and -13 display analgesic activity that is probably not due to endogenous opioid release, and could be related to a peripheral mechanism, probably via the inhibition of the release of the pro-inflammatory cytokines TNF-α and IL-1β by resident peritoneal macrophages.

Cytokine involvement in dynorphin-induced allodynia

Bupivacaine’s Action on the Carrageenan-Induced Inflammatory Response in Mice: Cytokine Production by Leukocytes After Ex-Vivo Stimulation

These experiments show that carrageenan-induced hindpaw inflammation modifies the blood cell reactivity to LPS and SAC and that bupivacaine regulates the systemic response elicited by carrageanan.



Bradykinin initiates cytokine‐mediated inflammatory hyperalgesia

Data show that bradykinin can initiate the cascade of cytokine release that mediates hyperalgesic responses to carrageenin and endotoxin, and suggests that the release of hyperAlgesic cytokines can be initiated independently of bradyKinin BK2 receptors.

The pivotal role of tumour necrosis factor alpha in the development of inflammatory hyperalgesia.

The delineation of the role of TNF alpha,IL-1 beta, 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 ofinflammatory hyperalGESia.

Interleukin‐8 as a mediator of sympathetic pain

IL‐8 is the first endogenous mediator to be identified as evoking hyperalgesia involving the sympathetic nervous system, and a new biological activity of IL-8 is described, namely the capacity to evoke hyperAlgesia by a prostaglandin‐independent mechanism.

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

An analgesic tripeptide analogue of IL-1β is developed which antagonizes hyperalgesia evoked by IL- 1β and by the inflammatory agent carrageenan.


The multiple facets of r IL-10 in experimental immunopathology indicate that the success of clinical trials with rIL-10 will depend both on the appropriate selection of the patient populations to be treated and on the early detection of possible adverse effects.

Interleukin 10 suppression of monocyte prostaglandin H synthase-2. Mechanism of inhibition of prostaglandin-dependent matrix metalloproteinase production.

Nuclear run-on transcription assays performed on monocytes exposed to ConA or the combination of ConA and IL-10 indicated thatIL-10 treatment suppressed PGHS-2 expression at the level of transcription, and the ability of exogenously added PGE2 or dibutyryl cAMP to restore the production of MMPs in IL- 10-treated monocytes was supported.

Interleukin 10(IL-10) inhibits cytokine synthesis by human monocytes: an autoregulatory role of IL-10 produced by monocytes

The results indicate that IL-10 has important regulatory effects on immunological and inflammatory responses because of its capacity to downregulate class II MHC expression and to inhibit the production of proinflammatory cytokines by monocytes.

IL-10 inhibits cytokine production by activated macrophages.

The potent action of IL-10 on the macrophage, particularly at the level of monokine production, supports an important role for this cytokine not only in the regulation of T cell responses but also in acute inflammatory responses.

Interleukin-1-induced prostaglandin E2 biosynthesis in human synovial cells involves the activation of cytosolic phospholipase A2 and cyclooxygenase-2.

The data suggest that the IL-1-induced production of PGE2 in human synoviocytes can be attributed to the stimulation of both cPLA2 and cyclooxygenase-2, which may represent appropriate targets for selective blockade of prostanoid production in the inflammed joints.

IL-10, T lymphocyte inhibitor of human blood cell production of IL-1 and tumor necrosis factor.

A factor is identified that inhibits the production of IL-1 beta and TNF by stimulated human mononuclear cells and use of mAb specifically showed the inhibitor to be IL-10, which inhibits T cell cytokine production.