Nasal hyperosmolar challenge with a dry powder of mannitol in patients with allergic rhinitis. Evidence for epithelial cell involvement

Koskela, Heikki; Sciascio, Maria Bernadette Di; Anderson, Sandra D.; Andersson, Morgan; Chan, Hak‐Kim; Gadalla, Shahinaz M.; Katelaris, Constance H.

doi:10.1046/j.1365-2222.2000.00923.x

Cited by 38 publications

(25 citation statements)

References 35 publications

(54 reference statements)

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“…2). Hyperosmolar challenge initiates the release of 15S-HETE in nasal lavage fl uid [29] and in nasal polyp cells in vitro. We found that relative to nonasthmatics, the level of 15S-HETE in the airways is increased after exercise challenge in asthmatics with EIB [30••].…”

Section: Role Of Leukotrienes In the Pathophysiology Of Eibmentioning

confidence: 99%

Role of leukotrienes in exercise-induced bronchoconstriction

Hallstrand

Henderson²

2008

Curr Allergy Asthma Rep

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Exercise-induced bronchoconstriction (EIB) refers to acute airflow obstruction that is triggered by a period of physical exertion. EIB occurs mainly in individuals with other features of asthma but is especially prominent in a subset of asthmatics with pronounced indirect airway hyperresponsiveness. Leukotrienes (LTs) play a critical role in the pathophysiology of EIB. Asthmatics who are susceptible to EIB have increased levels of cysteinyl LTs (cysLTs [ie, LTs C4, D4, and E4]) in induced sputum and exhaled breath condensate. Exercise challenge in individuals susceptible to this disorder initiates the sustained increase in cysLTs in the airways and an increase in the ratio of cysLTs to prostaglandin E(2). The effects of cysLTs leading to secreted mucin release and smooth muscle constriction may be mediated in part through activation of sensory nerves. Therapies that block cysLT production or the cysLT(1) receptor effectively reduce the severity of EIB.

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Section: Role Of Leukotrienes In the Pathophysiology Of Eibmentioning

confidence: 99%

Role of leukotrienes in exercise-induced bronchoconstriction

Hallstrand

Henderson²

2008

Curr Allergy Asthma Rep

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“…Nasal insufflation with chemokines, such as IL-8, 26 eotaxin, 27 and regulated on activation normally T-cell expressed and secreted (RANTES), 28 has also been used to evaluate the effect and time course of their effect on cell recruitment into the nasal lumen. Studies have also been undertaken to investigate the effects of non-IgE-related stimuli, such as hyperosmolar challenge, aspirin, and sodium metabisulfite, on mediator release within the nose, [29][30][31][32] and with or without therapeutic intervention, to gain insight into the magnitude of effect and mechanism of action of differing pharmacologic modalities on cell recruitment, cell activation, and induced vascular permeability. [33][34][35][36][37][38][39][40][41] Although these approaches have been widely used in the limited research setting, they have been less widely applied as a means of objectively monitoring nasal disease in the clinical trial setting.…”

Section: Nasal Lavagementioning

confidence: 99%

Objective monitoring of nasal airway inflammation in rhinitis

Howarth

Persson²,

Meltzer

et al. 2005

Journal of Allergy and Clinical Immunology

127

151

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“…It may be argued that the hyperosmotic medium itself could cause ␣ 2 M release. However, this seems unlikely since hyperosmotic mannitol failed to cause significant release of ␣ 2 M from human epithelial cells (49). In addition to liver cells and astroglia, blood cells may also produce ␣ 2 M (50).…”

Section: Fig 2 Radial Immunodiffusion Analysis Demonstrating Increamentioning

confidence: 99%

Blood-Brain Barrier Damage Induces Release of α2-Macroglobulin

Cucullo

Marchi

Marroni

et al. 2003

Molecular & Cellular Proteomics

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Blood-brain barrier (BBB) failure occurs in many neurological diseases and is caused in part by activation of proinflammatory factors including matrix metalloproteinases. Counterbalancing, "BBB protective" cascades have recently been described, including NO-mediated interleukin 6 release by glia. Interleukin 6 has been shown to trigger production of matrix metalloproteinase inhibitors such as ␣ 2 -macroglobulin (␣ 2 M). We hypothesized that BBB failure may result in increased ␣ 2 M release by perivascular astrocytes. This was initially tested in patients undergoing iatrogenic BBB disruption by hyperosmotic mannitol for intra-arterial chemotherapy of brain tumors. Serum samples revealed significantly increased levels of ␣ 2 M at 4 h after BBB disruption by hyperosmotic mannitol. In parallel in vitro experiments, we observed a similar increase of ␣ 2 M release by astrocytes under conditions mimicking BBB failure and perivascular edema. For both experiments, protein analysis was initially performed by bidimensional gel electrophoresis and mass spectrometry followed by Western blotting immunodetection. We conclude that, in addition to proinflammatory changes, BBB failure may also trigger protective release of ␣ 2 M by perivascular astrocytes as well as peripheral source.

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Nasal hyperosmolar challenge with a dry powder of mannitol in patients with allergic rhinitis. Evidence for epithelial cell involvement

Abstract: Epithelial cell seems to be involved with the mediator response to airway hyperosmolar challenge. The roles of sensory c-fibre nerve cell and mast cell remained less clear.

Cited by 38 publications

References 35 publications

Role of leukotrienes in exercise-induced bronchoconstriction

Role of leukotrienes in exercise-induced bronchoconstriction

Objective monitoring of nasal airway inflammation in rhinitis

Blood-Brain Barrier Damage Induces Release of α2-Macroglobulin

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