Systemic Glucocorticoid Therapy Reduces Pain and the Number of Endoneurial Tumor Necrosis Factor-Alpha (TNFα)-Positive Mast Cells in Rats With a Painful Peripheral Neuropathy

Hayashi, Reiko; Xiao, Wen; Kawamoto, Masashi; Yuge, Osafumi; Bennett, Gary J.

doi:10.1254/jphs.fp0072181

Cited by 45 publications

(31 citation statements)

References 37 publications

(31 reference statements)

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“…Pharmacological treatments that failed to decrease these levels included monotherapy of paracetamol, tramadol, cannabidiol, morphine, soluble TNF receptor, and IL-1 receptor antagonist. On the other hand, successful interventions that lower TNF- α expression included NMDA receptor antagonist MK-801, thalidomide, combined therapy of soluble TNF receptor with IL-1 receptor antagonist, chronic administration of morphine (dose-dependant with aggravation after interruption), α2-macroglobulin, nimesulide, a combination of paracetamol with tramadol, recombinant human erythropoietin and triamcinolone [32, 34–36, 43, 45, 55, 61, 62, 64]. …”

Section: Resultsmentioning

confidence: 99%

Role of TNF-alpha during central sensitization in preclinical studies

et al. 2011

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Tumor necrosis factor-alpha (TNF-α) is a principal mediator in pro-inflammatory processes that involve necrosis, apoptosis and proliferation. Experimental and clinical evidence demonstrate that peripheral nerve injury results in activation and morphological changes of microglial cells in the spinal cord. These adjustments occur in order to initiate an inflammatory cascade in response to the damage. Between the agents involved in this reaction, TNF-α is recognized as a key player in this process as it not only modulates lesion formation, but also because it is suggested to induce nociceptive signals. Nowadays, even though the function of TNF-α in inflammation and pain production seems to be generally accepted, diverse sources of literature point to different pathways and outcomes. In this review, we systematically searched and reviewed original articles from the past 10 years on animal models of peripheral nervous injury describing TNF-α expression in neural tissue and pain behavior.

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Section: Resultsmentioning

confidence: 99%

Role of TNF-alpha during central sensitization in preclinical studies

et al. 2011

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“…Glucocorticoids, which broadly and nonspecifically suppress the immune response, are commonly used in clinical practice to alleviate neuropathic pain in conditions such as lumbar radiculopathy and to prevent inflammation following nerve damage, such as spinal cord injury [104,105]. They have also been found to prevent development of neuropathic pain [106], possibly through a decrease in TNF-α concentrations in mast cells [107]. However, despite a number of clinical trials for various conditions, the true clinical effectiveness of glucocorticoids for neuropathic pain remains unclear [108].…”

Section: Alternative Approaches To Reduce Neuroinflammmationmentioning

confidence: 99%

Targeting cytokines for treatment of neuropathic pain

Hung

Lim

Doshi

2017

Scandinavian Journal of Pain

140

120

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AbstractBackgroundNeuropathic pain is a challenging condition often refractory to existing therapies. An increasing number of studies have indicated that the immune system plays a crucial role in the mediation of neuropathic pain. Exploration of the various functions of individual cytokines in neuropathic pain will provide greater insight into the mechanisms of neuropathic pain and suggest potential opportunities to expand the repertoire of treatment options.MethodsA literature review was performed to assess the role of pro-inflammatory and antiinflammatory cytokines in the development of neuropathic pain. Both direct and indirect therapeutic approaches that target various cytokines for pain were reviewed. The current understanding based on preclinical and clinical studies is summarized.Results and conclusionsIn both human and animal studies, neuropathic pain has been associated with a pro-inflammatory state. Analgesic therapies involving direct manipulation of various cytokines and indirect methods to alter the balance of the immune system have been explored, although there have been few large-scale clinical trials evaluating the efficacy of immune modulators in the treatment of neuropathic pain. TNF-α is perhaps the widely studied pro-inflammatory cytokine in the context of neuropathic pain, but other pro-inflammatory (IL-1β, IL-6, and IL-17) and anti-inflammatory (IL-4, IL-10, TGF-β) signaling molecules are garnering increased interest. With better appreciation and understanding of the interaction between the immune system and neuropathic pain, novel therapies may be developed to target this condition.

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“…31 We cannot yet state that the mechanisms of proinflammatory cytokines associated with the regulation of thoracotomy and rib retraction induced neuropathic pain, but increased TNF-α was shown in Schwann cells and mast cells of the injured sciatic nerve in rats after peripheral nerve injury. 45 Furthermore, activation of local Schwann cells is followed by increased production of TNF-α and IL-1β. 46 In this direction, it is believed that anti-inflammatory cytokines and proinflammatory cytokine inhibitors reduce neuropathic pain.…”

Section: Time Frame Of Mechanical Testingmentioning

confidence: 99%