Interleukin-1 antagonizes morphine analgesia and underlies morphine tolerance

@article{Shavit2005Interleukin1AM,
  title={Interleukin-1 antagonizes morphine analgesia and underlies morphine tolerance},
  author={Yehuda Shavit and Gilly Wolf and Inbal Goshen and Dina Livshits and Raz Yirmiya},
  journal={Pain},
  year={2005},
  volume={115},
  pages={50-59}
}

Figures from this paper

Evidence that opioids may have toll-like receptor 4 and MD-2 effects

Proinflammatory cytokines oppose opioid-induced acute and chronic analgesia

Interleukin‐1 System in CNS Stress

The ability of patients to mount an IL‐1ra response, as measured in the CSF, strongly correlated with the neurological outcome of traumatic brain injury (TBI), suggests selective induction or pharmacological application of IL-1ra may be sparing neurons in seizures and neurotrauma.

Chronic morphine treatment increased the expression of myeloid differentiation primary response protein 88 in rat spinal cord.

This study demonstrated that chronic intrathecal morphine injection led to a robust increase of MyD88 expression in rat spinal cord, and hypothesis the possible involvement of myeloid differentiation primary response protein 88 (MyD88), a key adaptor protein for the TLR and IL-1R families, in the development of tolerance to morphine-induced analgesia.

Opioid-Induced Glial Activation: Mechanisms of Activation and Implications for Opioid Analgesia, Dependence, and Reward

Data indicate that attenuation of glial activation, by general or selective TLR antagonistic mechanisms, may also be a clinical method for separating the beneficial and unwanted actions of opioids, thereby improving the safety and efficacy of their use.

Blockade of IL-18 signaling diminished neuropathic pain and enhanced the efficacy of morphine and buprenorphine

Interleukin-1 beta-induced up-regulation of opioid receptors in the untreated and morphine-desensitized U87 MG human astrocytoma cells

The results indicate that the pro-inflammatory cytokine, IL-1β, affects opiate-dependent pathways by up-regulating the expression of the MOR in both untreated and morphine-desensitized U87 MG.
...

References

SHOWING 1-10 OF 56 REFERENCES

The immunosuppressive effects of chronic morphine treatment are partially dependent on corticosterone and mediated by the μ‐opioid receptor

Results clearly show that morphine‐induced immunosuppression is mediated by the MOR and that although some functions are amplified in the presence of CORT or sympathetic activation, the inhibition of IFN‐γ synthesis and activation of macrophage‐cytokine synthesis is CORT‐independent and only partially dependent on sympathetic activation.

Cytokine‐mediated inflammatory hyperalgesia limited by interleukin‐1 receptor antagonist

IL‐1ra, released at sites of inflammation, limits inflammatory hyperalgesia and appears to be the result of antagonism by IL‐ 1ra of IL‐1β‐stimulated eicosanoid production.

A Role for Proinflammatory Cytokines and Fractalkine in Analgesia, Tolerance, and Subsequent Pain Facilitation Induced by Chronic Intrathecal Morphine

Results suggest that IL-1 and fractalkine are endogenous regulators of morphine analgesia and are involved in the increases in pain sensitivity that occur after chronic opiates.

Expression of interleukin‐1 receptors and their role in interleukin‐1 actions in murine microglial cells

Interestingly, a neutralizing antibody to IL‐1RII significantly increased the concentration ofIL‐1β in the medium of LPS‐treated microglia and exacerbated the IL‐ 1β‐induced IL‐6 release in mixed glia, providing the first evidence that microglial IL‐2RII regulates IL‐3β actions by binding excess levels of this cytokine during brain inflammation.

Impaired interleukin‐1 signaling is associated with deficits in hippocampal memory processes and neural plasticity

The results suggest that IL‐1 contributes to the regulation of memory processes as well as short‐ and long‐term plasticity within the hippocampus, which has important implications to several conditions in humans, which are associated with long-term defects inIL‐1 signaling.

Morphine enhances interleukin‐12 and the production of other pro‐inflammatory cytokines in mouse peritoneal macrophages

The enhancement of IL‐12 at both the mRNA and protein levels was antagonized by naltrexone, indicating that the modulation of this cytokine by morphine is via a classic opioid receptor.

Augmented production of proinflammatory cytokines and accelerated allotransplantation reactions in heroin‐treated mice

The results show that heroin treatment augments production of proinflammatory cytokines and accelerates allotransplantation reactions, illustrating the complexity of the effects of heroin on the immune system and should be taken into account during medical treatment of opiate addicts and in the use of morphine to decrease pain in various clinical situations.

Contribution of interleukin‐1β to the inflammation‐induced increase in nerve growth factor levels and inflammatory hyperalgesia

It is demonstrated that IL‐1β contributes to the upregulation of NGF during inflammation and that NGF has a major role in the production of inflammatory pain hypersensitivity.

A neuromodulatory role of interleukin-1β in the hippocampus

It is shown for the first time that the production of biologically significant amounts of IL-1β in the brain can be induced by a sustained increase in the activity of a discrete population of neurons and a physiological involvement of this cytokine in synaptic plasticity is suggested.
...