Nerve growth factor localization in the nasal mucosa of patients with persistent allergic rhinitis

Bresciani, M; Laliberté, François; Laliberté, Marie-France; Gramiccioni, Claudia; Бонини, С.

doi:10.1111/j.1398-9995.2008.01831.x

Cited by 33 publications

(22 citation statements)

References 43 publications

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“…Furthermore, allergic inflammation induced by nasal allergen exposure augments this 'naso-nasal' reflex [31]. Possible mechanisms for sensory nerve hyperresponsiveness include the increased release of nerve growth factor during allergic inflammation [32].…”

Section: Onset Of Three Major Ar Symptomsmentioning

confidence: 99%

Mechanisms and clinical implications of glucocorticosteroids in the treatment of allergic rhinitis

Okano

2009

Clinical and Experimental Immunology

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SummaryAllergic rhinitis is a common airway disease characterized by hypersensitivity, exudation, hypersecretion, inflammatory cell infiltration and remodelling. Intranasal glucocorticosteroids are the most effective drugs for controlling the inflammation caused by allergic rhinitis. Glucocorticosteroids exert anti-inflammatory effects through at least two pathways: the transactivation pathway and the transrepression pathway. Glucocorticosteroids also exert regulatory functions by inducing regulatory cytokines and forkhead box P3 (FoxP3 + ) regulatory T cells. Evidence suggests that intranasal glucocorticosteroids control not only nasal symptoms but also ocular symptoms. In contrast to sedating H1 receptor antagonists, intranasal glucocorticosteroids can improve impaired performance symptoms, such as daytime sleepiness, associated with allergic rhinitis. Recent studies suggest that intranasal glucocorticosteroids might also be useful for the prophylactic treatment of pollinosis; this possibility is supported by the molecular mechanism of the anti-inflammatory action of glucocorticosteroids. These findings suggest that intranasal glucocorticosteroids might be positioned as first-line drugs for the treatment of both perennial and seasonal allergic rhinitis.

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Section: Onset Of Three Major Ar Symptomsmentioning

confidence: 99%

Mechanisms and clinical implications of glucocorticosteroids in the treatment of allergic rhinitis

Okano

2009

Clinical and Experimental Immunology

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“…Sensory neuropeptides, such as tachykinins (SP and NKA), act via neurokinin 1 receptor (NK1R), neurokinin 2 receptor (NK2R), and MrgX2, a newly discovered receptor belonging to the mas-related gene family (MrgX receptors), whereas CGRP activates the CGRP receptor (CGRPR) [21][22][23] . Reciprocally, a variety of molecules including histamine, serotonin, and NGF, which are synthesized and released by MCs, can influence neuronal activity as well as the release of neuropeptides [24][25][26] . Additionally, proteaseactivated receptor 2 (PAR2) and the histamine receptor have also been found on trigeminal neurons in animals [27,28] .…”

Section: Increase Of Mastmentioning

confidence: 99%

Increase of Mast Cell-Nerve Association and Neuropeptide Receptor Expression on Mast Cells in Perennial Allergic Rhinitis

Le¹,

Schmit²,

Heck³

et al. 2016

Neuroimmunomodulation

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Objectives: Mast cells (MCs) and nerves play an important role in allergic rhinitis (AR), but little is known about their crosstalk in AR. The aim of this study was to investigate MC-nerve interaction in the human nasal mucosa during AR. Methods: The association between MCs and nerves, the expression of neuropeptide receptors (neurokinin 1 receptor [NK1R], neurokinin 2 receptor [NK2R], calcitonin gene-related peptide receptor [CGRPR], and MrgX2) on MCs, and protease-activated receptor 2 (PAR2) and tyrosine receptor kinase A (TrkA) on nerve fibres in the human nasal mucosa were investigated with immunofluorescence and real-time PCR. Results: The association between MCs and nerves was found to be significantly increased, although the numbers of MCs and nerve fibres were unchanged during AR. MCs expressing tryptase-chymase (MC_tc) were frequently associated with nerve fibres and these contacts increased significantly in AR. Neuropeptide receptors NK1R, NK2R, and CGRPR were firstly found to be largely localised on MCs. The number of MCs expressing NK1R and NK2R, but not CGRPR, was significantly increased in AR. Interestingly, MC_tc mostly expressed these neuropeptide receptors. The newly discovered tachykinin receptor MrgX2 was not expressed on nasal MCs, but was expressed on gland cells and increased in AR. Additionally, tachykinergic nerve fibres were found to express PAR2 or TrkA as receptors for MCs. Conclusions: This study revealed for the first time an increase of MC-nerve association and neuropeptide receptor expression on MCs during AR as well as nerve fibres containing receptors for MCs. These results suggest that targeting or controlling airway sensory nerve function as a modulator of MCs may prevent allergic airway inflammation such as AR.

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“…For this reason, nasal allergy progressed in connection with sensitization as a result of nerve elongation to the nasal dermis. In human patients with nasal rhinitis, detectable levels of nerve growth factor (NGF) increase in the nasal mucosa, and the sensory nerve is extended to the dermis [21]. However, mice that received repeated doses of 5-ASA did not acquire sensitivity to histamine due to protection from destruction of the barrier function of the nasal mucosa.…”

Section: Discussionmentioning

confidence: 99%

Effect of 5-aminosalicylate on allergic rhinitis model in mice

Kuyama

Yamamoto

Sugiyama

et al. 2010

International Immunopharmacology

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Nerve growth factor localization in the nasal mucosa of patients with persistent allergic rhinitis

Cited by 33 publications

References 43 publications

Mechanisms and clinical implications of glucocorticosteroids in the treatment of allergic rhinitis

Mechanisms and clinical implications of glucocorticosteroids in the treatment of allergic rhinitis

Increase of Mast Cell-Nerve Association and Neuropeptide Receptor Expression on Mast Cells in Perennial Allergic Rhinitis

Effect of 5-aminosalicylate on allergic rhinitis model in mice

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