Nociception and role of immune system in pain

Verma, Vivek; Sheikh, Zeeshan; Ahmed, Ahad S.

doi:10.1007/s13760-014-0411-y

Cited by 49 publications

(45 citation statements)

References 63 publications

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“…Pain, while a necessary response to prevent irreparable injury, can be a perplexing condition to resolve when it occurs chronically or without obvious provocation 71 . Pain can affect nearly any body site or it can be generalized; the effects of chronic pain are crippling, even when the pain is not associated with any life-threatening or physically debilitating condition 71 .…”

Section: Introductionmentioning

confidence: 99%

“…Pain can affect nearly any body site or it can be generalized; the effects of chronic pain are crippling, even when the pain is not associated with any life-threatening or physically debilitating condition 71 . While some chronic pain conditions (e.g.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, we have demonstrated that fibroblast production of proinflammatory mediators can accurately predict the pain threshold measured at the site of fibroblast origin 23 . Therefore, like many other chronic pain conditions, LPV appears to have inflammatory origins 71 .…”

Section: Introductionmentioning

confidence: 99%

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A Role for Bradykinin Signaling in Chronic Vulvar Pain

Falsetta

Foster

Woeller

et al. 2016

The Journal of Pain

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Chronic vulvar pain is alarmingly common in women of reproductive age and is often accompanied by psychological distress, sexual dysfunction, and a significant reduction in quality of life. Localized provoked vulvodynia (LPV) is associated with intense vulvar pain concentrated in the vulvar vestibule (area surrounding vaginal opening). To date, the origins of vulvodynia are poorly understood, and treatment for LPV manages pain symptoms, but does not resolve the root causes of disease. Until recently, no definitive disease mechanisms had been identified; our work indicates LPV has inflammatory origins, although additional studies are needed to understand LPV pain. Bradykinin signaling is one of the most potent inducers of inflammatory pain and is a candidate contributor to LPV. We report that bradykinin receptors are expressed at elevated levels in LPV patient versus healthy control vestibular fibroblasts, and patient vestibular fibroblasts produce elevated levels of proinflammatory mediators with bradykinin stimulation. Inhibiting expression of one or both bradykinin receptors significantly reduces proinflammatory mediator production. Finally, we determined that bradykinin activates NFκB signaling (a major inflammatory pathway), while inhibition of NFκB successfully ablates this response. These data suggest that therapeutic agents targeting bradykinin sensing and/or NFκB may represent new, more specific options for LPV therapy. Perspective: There is an unmet need for the development of more effective vulvodynia therapies. As we explore the mechanisms by which human vulvar fibroblasts respond to proinflammatory/pro-pain stimuli, we move closer to understanding the origins of chronic vulvar pain and identifying new therapeutic targets, knowledge which could significantly improve patient care.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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A Role for Bradykinin Signaling in Chronic Vulvar Pain

Falsetta

Foster

Woeller

et al. 2016

The Journal of Pain

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“…The innate immune response plays a critical role in central sensitization and in establishing acute pain [3], while the adaptive immune responses mediated by CD4 + T lymphocyte Cheng-ye Yao, Ze-lin Weng and Jian-cheng Zhang contributed equally to this work. infiltrated into the spinal cord are associated with the maintenance of neuropathic pain [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-17A Acts to Maintain Neuropathic Pain Through Activation of CaMKII/CREB Signaling in Spinal Neurons

Yao

Weng²,

Zhang

et al. 2015

Mol Neurobiol

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Immunity and neuroinflammation play major roles in neuropathic pain. Spinal interleukin (IL)-17A, as a mediator connecting innate and adaptive immunity, has been shown to be an important cytokine in neuroinflammation and acute neuropathic pain. However, the effects and underlying mechanisms of spinal IL-17A in the maintenance of neuropathic pain remain unknown. This study was designed to investigate whether spinal IL-17A acted to maintain neuropathic pain and to elucidate the underlying mechanisms in IL-17A knockout or wild-type (WT) mice following L4 spinal nerve ligation (L4 SNL). WT mice were treated with anti-IL-17A neutralized monoclonal antibody (mAb) or recombinant IL-17A (rIL-17A). We showed that IL-17A levels were significantly increased 1, 3, 7, and 14 days after SNL in spinal cord. Double immunofluorescence staining showed that astrocytes were the major cellular source of spinal IL-17A. IL-17A knockout or anti-IL-17A mAb treatment significantly ameliorated hyperalgesia 7 days after SNL, which was associated with a significant reduction of p-CaMKII and p-CREB levels in spinal cord, whereas rIL-17A treatment conferred the opposite effects. Furthermore, we showed that blocking CaMKII with KN93 significantly reduced SNL- or rIL-17A-induced hyperalgesia and p-CREB expression. Our in vitro data showed that KN93 also significantly inhibited rIL-17A-induced CREB activation in primary cultured spinal neurons. Taken together, our study indicates that astrocytic IL-17A plays important roles in the maintenance of neuropathic pain through CaMKII/CREB signaling pathway in spinal cord, and thus targeting IL-17A may offer an attractive strategy for the treatment of chronic persistent neuropathic pain.

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“…The pain induction is caused by the release of certain endogenous substances e.g. bradykinin and also from the production of pain mediators like arachidonic acid via cyclo-oxygenase pathway and prostaglandin synthesis (Verma et al, 2015). Abdominal writhing usually involves certain pain receptors which are located in the peritoneum (Mbiantcha et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

In-vivo evaluation of analgesic, anti-inflammatory and anti-pyretic activity of aqueous methanolic extract of Jatropha gossypifolia

Ghauri¹,

Khan²,

Khan³

et al. 2017

Afr. J. Pharm. Pharmacol.

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Many pathological conditions are associated with pain, fever and inflammation. Synthetic drugs available for the treatment of these ailments accompany many unwanted side effect; most prominent of which is the gastric ulcer. Present study was thus aimed at evaluating the analgesic, anti-pyretic and anti-inflammatory potential of aqueous methanolic extract of leaves of plant Jatropha gossypifolia. Antiinflammatory activity was evaluated using carrageenan induced paw edema. Acetic acid induced writhing test and hot plate method was used to assess the analgesic activity. Anti-pyretic activity was ascertained using brewer's yeast induced pyrexia. The aqueous methanolic extract of the plant J. gassypifolia have demonstrated significant analgesic, anti-pyretic and anti-inflammatory activity at 200 mg/kg dose. The data was statistically analyzed by one way ANOVA followed by post hoc Dunnett's test for multiple comparisons. It has thus concluded that aqueous methanolic extract of leaves of plant J. gassypifolia possess analgesic, anti-inflammatory and anti-pyretic properties. These results strongly support the ethno-pharmacological use of this plant as anti-pyretic, analgesic and anti-inflammatory agent.

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Nociception and role of immune system in pain

Cited by 49 publications

References 63 publications

A Role for Bradykinin Signaling in Chronic Vulvar Pain

A Role for Bradykinin Signaling in Chronic Vulvar Pain

Interleukin-17A Acts to Maintain Neuropathic Pain Through Activation of CaMKII/CREB Signaling in Spinal Neurons

In-vivo evaluation of analgesic, anti-inflammatory and anti-pyretic activity of aqueous methanolic extract of Jatropha gossypifolia

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