Tumour necrosis factor α mediates transient receptor potential vanilloid 1-dependent bilateral thermal hyperalgesia with distinct peripheral roles of interleukin-1β, protein kinase C and cyclooxygenase-2 signalling

Russell, Fiona A.; Fernandes, Elizabeth S.; Courade, Jean-Philippe; Keeble, Julie; Brain, Susan D.

doi:10.1016/j.pain.2009.01.021

Cited by 64 publications

(56 citation statements)

References 56 publications

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“…Bilateral thermal hyperalgesia was TRPV1-dependent and relies on IL-1β in the periphery. And the contralateral IL-1β acted back on the contralateral sensory nerves and sensitises TRPV1, resulting in the contralateral thermal hyperalgesia [34]. This phenomenon prompted that the activation of IL-1β may be involved either directly or indirectly in TRPV1 activation.…”

Section: Discussionmentioning

confidence: 99%

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Gao

Liu

Zhang

et al. 2016

Neuroscience Letters

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Section: Discussionmentioning

confidence: 99%

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Gao

Liu

Zhang

et al. 2016

Neuroscience Letters

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“…on June 7, 2019. by guest www.bloodjournal.org From elevated levels of pro-inflammatory cytokines including TNF-␣, IL-1␤, 12-HPETE, Endothelin-1, LTB-4, and PGE 2 . 31 TNF-␣ appears to initiate the inflammatory cytokine cascade that sensitizes TRPV1, 32 and 12-HPETE and LTB-4 are documented endogenous direct activators of TRPV1. 33 ET-1 is also known to sensitize TRPV1.…”

Section: Discussionmentioning

confidence: 99%

Transient receptor potential vanilloid 1 mediates pain in mice with severe sickle cell disease

Hillery

Kerstein

Vilceanu

et al. 2011

Blood

136

194

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Pain is the leading cause of emergency department visits, hospitalizations, and daily suffering in individuals with sickle cell disease (SCD). The pathologic mechanisms leading to the perception of pain during acute RBC sickling episodes and development of chronic pain remain poorly understood and ineffectively treated. We provide the first study that explores nociceptor sensitization mechanisms that contribute to pain behavior in mice with severe SCD. Sickle mice exhibit robust behavioral hypersensitivity to mechanical, cold, and heat stimuli. Mechanical hypersensitivity is further exacerbated when hypoxia is used to induce acute sickling. Behavioral mechanical hypersensitivity is mediated in part by enhanced excitability to mechanical stimuli at both primary afferent peripheral terminal and sensory membrane levels. In the present study, inhibition of the capsaicin receptor transient receptor potential vanilloid 1 (TRPV1) with the selective antagonist A-425619 reversed the mechanical sensitization at both primary afferent terminals and isolated somata, and markedly attenuated mechanical behavioral hypersensitivity. In contrast, inhibition of TRPA1 with HC-030031 had no effect on mechanical sensitivity. These results suggest that the TRPV1 receptor contributes to primary afferent mechanical sensitization and a substantial portion of behavioral mechanical hypersensitivity in SCD mice. Therefore, TRPV1-targeted compounds that lack thermoregulatory side effects may provide relief from pain in patients with SCD. (Blood. 2011;118(12):3376-3383) IntroductionSickle cell disease (SCD) is a major health care and socioeconomic problem that affects millions of people worldwide. In the United States alone, SCD affects Ͼ 80 000 people, the majority of whom are African American. Pain is the hallmark symptom of SCD and the leading cause of emergency department visits, hospitalizations, and daily suffering. 1 Patients suffer unpredictable, incapacitating acute pain episodes that are believed to result from red blood cell (RBC) sickling and "vaso-occlusion." However, many features of this pain are not explained by hemoglobin polymerization and vascular obstruction. Furthermore, individuals with SCD often develop chronic pain syndromes that are poorly understood and ineffectively treated. 1,2 The frequency and severity of pain is associated with increased mortality and profoundly erodes patients' quality of life. 3 Because they are often from minority and lower socioeconomic groups, SCD patients are commonly underserved and suboptimally treated.The pathologic mechanisms leading to the perception of pain during RBC sickling episodes and the transition from acute to chronic pain remain poorly understood. 1,2 Patient descriptors of SCD pain include neuropathic pain attributes such as "aching," "shooting," and "stabbing," as well as nociceptive pain qualities such as "sharp," "throbbing," and "pounding." These descriptors depict spontaneous pain or nonstimulus-evoked pain. 2,4 Furthermore, increased hospital admissions and reports of...

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“…Neutrophils are the most abundant immune cells, accounting for around 55-70% of all white blood cells, and are the dominant cell type in sites of inflammation in the first hours following infection or injury. Blockade of neutrophil migration using a polysaccharide selectin inhibitor (fucoidin) abolishes cytokine induced hyperalgesia [88,89]. Neutrophils have been shown to release NGF and prostaglandins, which act to sensitise the nociceptive system, as discussed above [88].…”

Section: Inflammatory Cellsmentioning

confidence: 98%

What We have Learned about Pain from Rodent Models of Arthritis?

Inglis¹,

Schutze²,

McNamee

2010

CRR

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Rheumatoid arthritis (RA) and Osteoarthritis (OA) are both common diseases of the joints. RA is distinguished by inflammation and synovitis leading to joint destruction, whereas OA is typified by degenerative and mostly noninflammatory disease. Although differing in their pathology, both forms can elicit chronic disabling pain in patients. Relief from this pain is an unmet need for many patients, and this has lead to a drive to understand the pain mechanisms occurring in each disease in order to develop new analgesics. This necessitates the use of pre-clinical models. Here we discuss the methods and limitations of animal pain assessment, rodent models of RA and OA, and how these models have been used to investigate the genesis of pain. Specifically, we focus on processes studied in both RA and OA models, and how the mediators involved in the development of pain may differ between these two arthritic states and during acute and chronic pain. From this we have learnt that the key mediators of RA pain include inflammatory cells, inflammatory cytokines, astrocytes, substance P, and CGRP. Endogenous analgesic mediators in RA include β-endorphin, µ-opioid receptor, and various anti-inflammatory cytokines. Less is known of the mediators of OA pain, but important factors include CGRP, TRPV1, NGF, VIP and the µ-opioid receptor. Interestingly, several factors have been found not to play a role in OA pain, including glial cells, neutrophils and TNF. It must be noted that the vast majority of candidate drugs from animal research never reach the human clinic, in part due to false positives from animal models. This may be due to flaws in the models themselves, the methods used to assess pain, the physical properties of the candidate drug, or an inherent difference between animal and human pain pathways. By developing more clinically relevant models, novel diseasespecific analgesics are being developed with the hope of improving the quality of life for sufferers of arthritis pain.

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Tumour necrosis factor α mediates transient receptor potential vanilloid 1-dependent bilateral thermal hyperalgesia with distinct peripheral roles of interleukin-1β, protein kinase C and cyclooxygenase-2 signalling

Cited by 64 publications

References 56 publications

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Transient receptor potential vanilloid 1 mediates pain in mice with severe sickle cell disease

What We have Learned about Pain from Rodent Models of Arthritis?

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