Extending the understanding of sensory neuropeptides

Swert, Katelijne O. De; Joos, Guy

doi:10.1016/j.ejphar.2005.12.066

Cited by 94 publications

(82 citation statements)

References 134 publications

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“…These sensory neuropeptides can act on a number of effector cells in the respiratory tract (e.g., airway smooth muscles, cholinergic ganglia, mucous glands, immune cells) and elicit the local "axon reflexes" such as protein extravasation, inflammatory cell chemotaxis, etc. (16,38). Therefore, it is believed that these C-fiber sensory nerves play an important part in the manifestation of various symptoms of airway hypersensitivity in patients with airway inflammatory diseases such as asthma, bronchitis, and viral infection (7,20,32,38).…”

Section: Discussionmentioning

confidence: 99%

Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-α in rat pulmonary sensory neurons

Gu²,

Lin³

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Hu Y, Gu Q, Lin RL, Kryscio R, Lee LY. Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-␣ in rat pulmonary sensory neurons. Am J Physiol Lung Cell Mol Physiol 299: L483-L492, 2010. First published July 16, 2010 doi:10.1152/ajplung.00111.2010.-TNF␣, a proinflammatory cytokine known to be involved in the pathogenesis of allergic asthma, has been shown to induce hyperalgesia in somatic tissue via a sensitizing effect on dorsal root ganglion neurons expressing transient receptor potential vanilloid type 1 receptor (TRPV1). Because TRPV1-expressing pulmonary sensory neurons play an important role in regulating airway function, this study was carried out to determine whether TNF␣ alters the sensitivity of these neurons to chemical activators. Responses of isolated nodose and jugular ganglion neurons innervating the rat lungs were determined by measuring the transient increase in intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i). Our results showed the following. 1) A pretreatment with TNF␣ (50 ng/ml) for ϳ24 h increased significantly the peak ⌬[Ca 2ϩ ]i evoked by capsaicin (Cap) in these neurons. A pretreatment with the same concentration of TNF␣ for a longer duration (ϳ48 h) did not further increase the response, but pretreatment for a shorter duration (1 h) or with a lower concentration (25 ng/ml, 24 h) failed to enhance the Cap sensitivity.2) The same TNF␣ pretreatment also induced similar but less pronounced and less uniform increases in the responses to acid (pH 6.5-5.5), 2-aminoethoxydiphenyl borate (2-APB), a common activator of TRPV1, V2, and V3 channels, and allyl isothiocyanate (AITC), a selective activator of TRPA1 channel. 3) In sharp contrast, the responses to ATP, ACh, and KCl were not affected by TNF␣. 4) The TNF␣-induced hypersensitivity to Cap was not prevented by pretreatment with indomethacin (30 M). 5) The immunoreactivity to both TNF receptor types 1 and 2 were detected in rat vagal pulmonary sensory neurons. In conclusion, prolonged treatment with TNF␣ induces a pronounced potentiating effect on the responses of isolated pulmonary sensory neurons to TRPV1 activators. This action of TNF␣ may contribute in part to the airway hyperresponsiveness induced by this cytokine. intracellular calcium; pulmonary afferent; transient receptor potential vanilloid type 1; airway inflammation; asthma AN IMPORTANT ROLE OF TNF␣ in the pathogenesis of allergic asthma has been extensively documented (6,9,28,47). TNF␣ can be released from a variety of cell types in the airways, particularly macrophages, monocytes, and mast cells. TNF␣, either newly synthesized or preformed and stored constitutively within the mast cell granules, is coreleased with other potent mediators such as histamine and tryptase via the IgE-dependent mechanism (9, 21, 47). TNF␣ was detected in bronchoalveolar lavage fluid, sputum, exhaled breath condensate, and serum of asthmatic patients during asthmatic attack or following antigen inhalation challenge (12,33,39). Furthermore, it has been shown that TNF␣ is releas...

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Section: Discussionmentioning

confidence: 99%

Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-α in rat pulmonary sensory neurons

Gu²,

Lin³

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…ный агент [6]. Источником SP служат макрофаги, эозинофилы, лимфоциты, дендритные клетки и мо ноциты [7]. SP всегда высвобождается в ответ на по вреждение слизистой оболочки [8].…”

Section: ключевые слова: риносинусит лицевая боль субстанция рunclassified

Role of substance P in the pathogenesis of facial pain in rhinosinusitis

Stagnieva¹

2015

Ross. rinol.

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“…Inhalation of the well-known TRPV1 agonist capsaicin consistently and reproducibly elicits cough in animals and humans [84][85][86]. TRPV1 receptors are found on sensory airway nerves that play important roles in the cough reflex [13,42,52,87]. Groneberg et al found a significant correlation between the capsaicin tussive response and the numbers of TRPV1 positive nerves in patients with chronic cough of diverse causes, suggesting that TRPV1 receptors contributed to the enhanced cough reflex [42].…”

Section: Coughmentioning

confidence: 99%

“…A c c e p t e d m a n u s c r i p t 13 In vitro studies using human bronchial epithelial cells have demonstrated increased production of pro-inflammatory cytokines, such as interleukin-6 and interleukin-8, and oncotic cell death associated with TRPV1 activation [37,98]. Other studies have also demonstrated that particulate matter increases intracellular Ca 2+ and induces apoptosis of cultured lung epithelial cells via activation of TRPV1 [38,99].…”

Section: Apoptosis and Trpv1mentioning

confidence: 99%

“…They have potent effects on the tone of airway smooth muscle, airway secretions, edema of airway mucosa and on inflammatory and immune cells that mediate neurogenic inflammation via binding tachykinin ligands (NK 1 , NK 2 and NK 3 ) or CGRP receptors [6][7][8][9][10][11][12][13][14]. Thus, responses evoked by activating C-fiber afferents are mediated both by central reflex pathways and by local or axon reflexes involving the release of tachykinins from sensory endings.…”

Section: Introductionmentioning

confidence: 99%

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Is TRPV1 a useful target in respiratory diseases?

Takemura

Quarcoo

Niimi

et al. 2008

Pulmonary Pharmacology & Therapeutics

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This review focuses on the transient receptor potential vanilloid 1 (TRPV1). TRPV1 is a non-selective cation channel predominantly expressed in the cell membranes of sensory afferent fibers, which are activated multi-modally. In the mammalian respiratory system, immunohistochemical and electrophysiological studies have revealed heterogeneous localizations of TRPV1 channels in the airways and their presence in pleural afferents. TRPV1 channels in afferents are not only involved with sensory inputs, but also release several neuropeptides upon stimulation. These processes trigger pathophysiological effects (e.g. reflex bronchoconstriction, hypersecretion, cough, etc.) that cause various symptoms of airway diseases.Recent studies have identified several endogenous and exogenous substances that can activate TRPV1 in the lung. Because of its key role in initiating inflammatory processes, TRPV1 receptor antagonists have been proposed as therapeutic candidates. Therefore, a critical update of recent therapeutic results is also given in this review.

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Extending the understanding of sensory neuropeptides

Cited by 94 publications

References 134 publications

Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-α in rat pulmonary sensory neurons

Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-α in rat pulmonary sensory neurons

Role of substance P in the pathogenesis of facial pain in rhinosinusitis

Is TRPV1 a useful target in respiratory diseases?

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