Endothelins contribute towards nociception induced by antigen in ovalbumin‐sensitised mice

Piovezan, Anna Paula; D’Orléans-Juste, Pedro; Frighetto, Mônica; Souza, Glória Emília Petto de; Henriques, Maria das Graças; Rae, Giles A.

doi:10.1038/sj.bjp.0705663

Cited by 41 publications

(44 citation statements)

References 56 publications

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“…*, significant difference from baseline (P Ͻ 0.001); #, significant differences from control mice (P Ͻ 0.001). 1998a), injected subcutaneously into the plantar surface of the hind paw, (Baamonde et al 2004;Balonov et al 2006;Gokin et al 2001;Houck et al 2004;Menendez et al 2003b;Piovezan et al 1998Piovezan et al , 2004Verri et al 2004Verri et al , 2005 or skin of the back (Mujenda et al 2007), and injected into tumor-bearing tissues Schmidt et al 2007;Wacnik et al 2001). In contrast, the newer ET A receptor-selective antagonists have been administered systemically (Chichorro et al 2006a;Klass et al 2005;Matwyshyn et al 2006;Piovezan et al 2000;Trentin et al 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Injection of ET-1 into the knee or hind paw evokes nocifensive behaviors in animals (Baamonde et al 2004;Balonov et al 2006;De-Melo et al 1998a;Ferreira et al 1989;McKelvy et al 2007;Piovezan et al 1998Piovezan et al , 2004Verri et al 2004Verri et al , 2005. For example, injection of ET-1 into the plantar surface of the hind paw evoked dose-dependent hind paw licking (Gokin et al 2001;Menendez et al 2003b;Piovezan et al 2000), and application of ET-1 directly to the sciatic nerve evoked robust hind paw flinching (Davar et al 1998;Fareed et al 2000).…”

Section: Et-1-evoked Nocifensive Behaviors and Hyperalgesiamentioning

confidence: 99%

“…Numerous studies have demonstrated that injection of ET-1 into the knee or hind paw evokes nocifensive behaviors (Baamonde et al 2004;Balonov et al 2006;De-Melo et al 1998a;Ferreira et al 1989;Gokin et al 2001;McKelvy et al 2007;Menendez et al 2003b;Piovezan et al 1998Piovezan et al , 2004Verri et al 2004Verri et al , 2005, tactile allodynia (Balonov et al 2006;McKelvy et al 2007), and mechanical (da Ferreira et al 1989) and heat (Menendez et al 2003b) hyperalgesia through a mechanism involving the ET A receptors located in peripheral tissues (Baamonde et al 2004;Davar et al 1998;De-Melo et al 1998a;Fareed et al 2000;Gokin et al 2001;Menendez et al 2003b;Piovezan et al 2000). Injection of ET-1 into the skin excites C nociceptors (Gokin et al 2001;Khodorova et al 2002;Namer et al 2007) and likely contributes to ET-1-evoked nocifensive behaviors.…”

Section: Introductionmentioning

confidence: 99%

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Tumor-Evoked Sensitization of C Nociceptors: A Role for Endothelin

Hamamoto

Khasabov

Cain

et al. 2008

Journal of Neurophysiology

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Hamamoto DT, Khasabov SG, Cain DM, Simone DA. Tumorevoked sensitization of C nonciceptos: a role for endothelin. J Neurophysiol 100: 2300 -2311, 2008. First published August 6, 2008 doi:10.1152/jn.01337.2007. Primary and metastatic cancers that effect bone are frequently associated with pain. Sensitization of primary afferent C nociceptors innervating tissue near the tumor likely contributes to the chronic pain and hyperalgesia accompanying this condition. This study focused on the role of the endogenous peptide endothelin-1 (ET-1) as a potential peripheral algogen implicated in the process of cancer pain. Electrophysiological response properties, including ongoing activity and responses evoked by heat stimuli, of C nociceptors were recorded in vivo from the tibial nerve in anesthetized control mice and mice exhibiting mechanical hyperalgesia following implantation of fibrosarcoma cells into and around the calcaneus bone. ET-1 (100 M) injected into the receptive fields of C nociceptors innervating the plantar surface of the hind paw evoked an increase in ongoing activity in both control and tumor-bearing mice. Moreover, the selective ET A receptor antagonist, BQ-123 (3 mM), attenuated tumor-evoked ongoing activity in tumor-bearing mice. Whereas ET-1 produced sensitization of C nociceptors to heat stimuli in control mice, C nociceptors in tumor-bearing mice were sensitized to heat, and their responses were not further increased by ET-1. Importantly, administration of BQ-123 attenuated tumor-evoked sensitization of C nociceptors to heat. We conclude that ET-1 at the tumor site contributes to tumor-evoked excitation and sensitization of C nociceptors through an ET A receptor mediated mechanism.

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Section: Discussionmentioning

confidence: 99%

Section: Et-1-evoked Nocifensive Behaviors and Hyperalgesiamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Tumor-Evoked Sensitization of C Nociceptors: A Role for Endothelin

Hamamoto

Khasabov

Cain

et al. 2008

Journal of Neurophysiology

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“…However, it is unknown how allergic inflammation causes neuropsychiatric dysfunction. We and others have reported the emergence of a peculiar form of myelitis presenting with persistent neuropathic pain, specifically allodynia, as a cardinal symptom in patients with atopic disorders, such as atopic dermatitis, allergic rhinitis, and atopic asthma, in Japan and Korea (Kira et al, 1997Murai et al, 2004;Ochi et al, 2004;Yoon et al, 2009;Ainiding et al, 2012;Kanamori et al, 2013). These patients with myelitis and atopy showed specific increases in C-C motif chemokine 11 and interleukin-9 in the CSF (Tanaka et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

“…Allergic disorders are associated with neuropsychiatric conditions, such as attention-deficit and hyperactivity disorder, autism spectrum disorder, and asthmatic amyotrophy (Hopkins' syndrome) (Hopkins, 1974;Roth et al, 1991;Liedholm et al, 1994;M.H. Chen et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Allergic Inflammation Leads to Neuropathic Pain via Glial Cell Activation

et al. 2016

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Allergic and atopic disorders have increased over the past few decades and have been associated with neuropsychiatric conditions, such as autism spectrum disorder and asthmatic amyotrophy. Myelitis presenting with neuropathic pain can occur in patients with atopic disorder; however, the relationship between allergic inflammation and neuropathic pain, and the underlying mechanism, remains to be established. We studied whether allergic inflammation affects the spinal nociceptive system. We found that mice with asthma, atopic dermatitis, or atopic diathesis had widespread and significantly more activated microglia and astroglia in the spinal cord than those without atopy, and displayed tactile allodynia. Microarray analysis of isolated microglia revealed a dysregulated phenotype showing upregulation of M1 macrophage markers and downregulation of M2 markers in atopic mice. Among the cell surface protein genes, endothelin receptor type B (EDNRB) was most upregulated. Immunohistochemical analysis revealed that EDNRB expression was enhanced in microglia and astroglia, whereas endothelin-1, an EDNRB ligand, was increased in serum, lungs, and epidermis of atopic mice. No EDNRA expression was found in the spinal cord. Expression of FBJ murine osteosarcoma viral oncogene homolog B was significantly higher in the dorsal horn neurons of asthma mice than nonatopic mice. The EDNRB antagonist BQ788 abolished glial and neural activation and allodynia. We found increased serum endothelin-1 in atopic patients with myelitis and neuropathic pain, and activation of spinal microglia and astroglia with EDNRB upregulation in an autopsied case. These results suggest that allergic inflammation induces diffuse glial activation, influencing the nociceptive system via the EDNRB pathway.

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Anti-allergic effects of natural tetranortriterpenoids isolated from Carapa guianensis Aublet on allergen-induced vascular permeability and hyperalgesia

et al. 2005

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Objective: We investigated the anti-allergic and analgesic properties of an oil and a derived fraction of tetranortriterpenoids (TNTP) obtained from the seeds of Carapa guianensis Aublet. Materials and methods: Pleurisy, paw and ear edema were induced in Swiss and C57/Bl10 mice mice, whereas thermal hyperalgesia was assessed in Wistar rats (n = 6 -10 per group). Values of p < 0.05 were regarded as significant. Results: C. guianensis oil (100 to 400 mg/kg, p. o.) and TNTP (12.5 to 100 mg/kg, p. o.) inhibited pleural exudation, paw and ear edema induced by ovalbumin (OVA) in sensitized mice. TNTP (12.5 to 100 mg/kg, p. o.) also inhibited paw edema induced by histamine, PAF and bradykinin. TNTP (100 mg/kg, p. o.) inhibited prostaglandin E 2 generation in the pleural cavity in response to antigenic challenge. Moreover, C. guianensis oil (100 to 400 mg/kg) and TNTP (12.5 to 100 mg/kg) decreased OVA-and histamine-induced hyperalgesia. Conclusion: Taken together, these findings demonstrate the anti-edematogenic and analgesic effects of C. guianensis oil, and points out TNTP as the responsible bioactive compounds.

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Endothelins contribute towards nociception induced by antigen in ovalbumin‐sensitised mice

Cited by 41 publications

References 56 publications

Tumor-Evoked Sensitization of C Nociceptors: A Role for Endothelin

Tumor-Evoked Sensitization of C Nociceptors: A Role for Endothelin

Allergic Inflammation Leads to Neuropathic Pain via Glial Cell Activation

Anti-allergic effects of natural tetranortriterpenoids isolated from Carapa guianensis Aublet on allergen-induced vascular permeability and hyperalgesia

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