The effect of platelet‐activating factor on the responsiveness of the human nasal airway

Austin, C.E.; Foreman, J. C.

doi:10.1111/j.1476-5381.1993.tb13779.x

Cited by 18 publications

(28 citation statements)

References 28 publications

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“…56 Human PAF nasal provocation leads to increased nasal airway resistance, reduced nasal volume, and symptoms of nasal obstruction. [57][58][59] Biochemically, PAF challenge results in nasal hyperresponsiveness to histamine and kinins and recruitment of neutrophils and eosinophils to the nasal mucosa. 58,60,61 PAFRs are expressed in nasal mucosal epithelial cells, submucosal glands, vascular endothelial cells, mast cells, leukocytes, and lymphocytes.…”

Section: Allergic Rhinitis and Asthmamentioning

confidence: 99%

“…[57][58][59] Biochemically, PAF challenge results in nasal hyperresponsiveness to histamine and kinins and recruitment of neutrophils and eosinophils to the nasal mucosa. 58,60,61 PAFRs are expressed in nasal mucosal epithelial cells, submucosal glands, vascular endothelial cells, mast cells, leukocytes, and lymphocytes. 62 In animal models of allergic rhinitis, PAFR antagonists reduce nasal airway resistance and vascular permeability after allergen challenge.…”

Section: Allergic Rhinitis and Asthmamentioning

confidence: 99%

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Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis

Gill

Jindal

Jagdis

et al. 2015

Journal of Allergy and Clinical Immunology

110

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Anaphylaxis is an acute, severe, life-threatening multisystem allergic reaction resulting from the sudden systemic release of biochemical mediators and chemotactic substances. Release of both preformed granule-associated mediators and newly generated lipid-derived mediators contributes to the amplification and prolongation of anaphylaxis. Platelet-activating factor (PAF) is a potent phospholipid-derived mediator the central role of which has been well established in experimental models of both immune-mediated and non-immune mediated anaphylaxis. It is produced and secreted by several types of cells, including mast cells, monocytes, tissue macrophages, platelets, eosinophils, endothelial cells, and neutrophils. PAF is implicated in platelet aggregation and activation through release of vasoactive amines in the inflammatory response, resulting in increased vascular permeability, circulatory collapse, decreased cardiac output, and various other biological effects. PAF is rapidly hydrolyzed and degraded to an inactive metabolite, lysoPAF, by the enzyme PAF acetylhydrolase, the activity of which has shown to correlate inversely with PAF levels and predispose to severe anaphylaxis. In addition to its role in anaphylaxis, PAF has also been implicated as a mediator in both allergic and nonallergic inflammatory diseases, including allergic rhinitis, sepsis, atherosclerotic disease, and malignancy, in which PAF signaling has an established role. The therapeutic role of PAF antagonism has been investigated for several diseases, with variable results thus far. Further investigation of its role in pathology and therapeutic modulation is highly anticipated because of the pressing need for more selective and targeted therapy for the management of severe anaphylaxis.

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Section: Allergic Rhinitis and Asthmamentioning

confidence: 99%

Section: Allergic Rhinitis and Asthmamentioning

confidence: 99%

Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis

Gill

Jindal

Jagdis

et al. 2015

Journal of Allergy and Clinical Immunology

110

View full text Add to dashboard Cite

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“…51 The re sulting AHR is similar, in many w ays, to that observe d in allergic rhinitis , as PAF also c ause s a signific ant nasal ne utrophilia and eosinophilia, toge the r w ith raise d ECP levels in nasal lavage fluid. [52][53][54] Although PAF c an induc e AHR in the human nasal airw ay, its role in allergen-induced AHR is less de fine d. Antige n challenge w ith grass polle n in atopic indiv iduals w ith SAR causes the release of lyso-PAF and PAF, 41,55 but it is uncle ar w he ther PAF or lyso-PAF are release d in PAR, 56 One possibility is that any PAF generate d is c onve rte d to lyso-PAF by acetylhydrolase present in the lavage fluid. The ac tivity of this enzyme in lavage fluid is signific antly rais ed follow ing grass polle n challenge in sensitive subje cts.…”

Section: Platelet Activating Factor (Paf)mentioning

confidence: 97%

“…50 In normal, non-atopic subjects, it induce s a nasal AHR to histamine and bradykinin 51,52 and causes an inc re ased re sponse to polle n in subjec ts w ith SAR. 51 The re sulting AHR is similar, in many w ays, to that observe d in allergic rhinitis , as PAF also c ause s a signific ant nasal ne utrophilia and eosinophilia, toge the r w ith raise d ECP levels in nasal lavage fluid.…”

Section: Platelet Activating Factor (Paf)mentioning

confidence: 99%

Hyperresponsiveness in the Human Nasal Airway: New Targets for the Treatment of Allergic Airway Disease

Turner

Foreman

1999

Mediators of Inflammation

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Allergic rhinitis is a condition which affects over 15% of the population in the United Kingdom. The pathological process involves two stages: nasal inflammation, and the development of nasal airway hyperresponsiveness (AHR) to allergen and a number of other stimuli. This results in the amplification of any subsequent allergic reaction, contributing to the chronic allergic state. A number of different hypotheses have been proposed to explain the underlying mechanism of AHR, including a role for eosinophil-derived proteins, free radicals and neuropeptides. While there may be a number of independent pathways which can result in AHR, evidence obtained from both animal models and in vivo experiments in humans indicate that some mediators may interact with one another, resulting in AHR. Further research into these interactions may open new avenues for the pharmacological treatment of chronic allergic rhinitis, and possibly other allergic airway diseases.

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“…We have investigated the possible involvement of PAF in allergic rhinitis, and have found that PAF can be released, along with its precursor/metabolite lyso-PAF, in nasal lavage fluids during the early antigen-induced reaction in patients with respiratory allergy [2]. Nasal challenge with PAF provokes nasal obstruction with an increase in nasal airway resistances [3], and nasal hyperreactivity [4,5]. Furthermore, nasal neutrophilia and eosinophilia have been observed after challenge with PAF, with a more rapid and more marked response in atopic than in normal subjects [6].…”

mentioning

confidence: 99%

Nasal eosinophilia induced by PAF-acether is accompanied by the release of eosinophil cationic protein

1994

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N Na as sa al l e eo os si in no op ph hi il li ia a i in nd du uc ce ed d b by y P PA AF F--a ac ce et th he er r i is s a ac cc co om mp pa an ni ie ed d b by y t th he e r re el le ea as se e o of f e eo os si in no op ph hi il l c ca at ti io on ni ic c p pr ro ot te ei in n A. Tedeschi, N. Milazzo, A. Miadonna Nasal eosinophilia induced by PAF-acether is accompanied by the release of eosinophil cationic protein. A. Tedeschi, N. Milazzo, A. Miadonna. ERS Journals Ltd 1994. ABSTRACT: It has been demonstrated that platelet-activating factor (PAF)-acether can induce nasal neutrophilia and eosinophilia, with a different degree of responsiveness in atopic and in nonatopic subjects. The aim of this study was to evaluate whether PAF can also induce the release of secondary mediators in the human nose. Ten patients with allergic rhinitis and 10 normal subjects underwent nasal challenge with PAF (500 nmol), lyso-PAF (500 nmol) and saline solution. Nasal lavages were performed before and after challenge to evaluate changes in nasal cytology and release of histamine, immunoreactive leukotriene (iLT) C 4 and eosinophil cationic protein (ECP).PAF caused neutrophilia and eosinophilia, which appeared earlier in atopic than in nonatopic subjects (30 min vs 1 h), and peaked 3 h after challenge in both groups. Lyso-PAF caused mild neutrophilia, which appeared 3 h after challenge in both groups; an increase in eosinophil counts was observed 3 h after challenge in atopic subjects, but not in nonatopic subjects. PAF insufflation caused a significant release of ECP in nasal lavage fluids 30 min and 3h after challenge in atopic subjects, and 3 h after challenge in nonatopic subjects. ECP levels in the nasal lavages collected 30 min and 3 h after challenge with PAF were higher in atopic than in nonatopic subjects. Eosinophil counts correlated with ECP levels in the nasal lavages collected 30 min after PAF challenge in atopic subjects. Nasal challenge with lyso-PAF did not provoke any release of ECP. No significant increase of histamine and iLTC 4 levels in nasal lavages was found after challenge with either PAF or lyso-PAF.These results indicate that PAF-induced nasal eosinophilia is accompanied by ECP release, which appears earlier and is more marked in atopic than in nonatopic subjects.

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The effect of platelet‐activating factor on the responsiveness of the human nasal airway

Cited by 18 publications

References 28 publications

Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis

Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis

Hyperresponsiveness in the Human Nasal Airway: New Targets for the Treatment of Allergic Airway Disease

Nasal eosinophilia induced by PAF-acether is accompanied by the release of eosinophil cationic protein

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