Regulation of Proinflammatory Cytokines in Seasonal Allergic Rhinitis

ENT Department, University Hospital Ghent, Belgium.
International Archives of Allergy and Immunology (Impact Factor: 2.67). 04/1999; 118(2-4):375-9. DOI: 10.1159/000024141
Source: PubMed


Mediators and cytokines have been demonstrated to be released due to nasal allergen exposure in sensitized subjects, but little is known about the release of cytokines and their antagonists under natural conditions.
Mediators - histamine, eosinophilic cationic protein (ECP), leukotrienes (LT) C4/ D4/E4 - and cytokines - interleukin (IL)-1beta, IL-8, IL-1 receptor antagonist (ra) - were measured in nasal secretions throughout the grass pollen season (6 visits) and for 6 weeks thereafter (3 visits) in patients with seasonal allergic rhinitis (n = 13) and compared to controls (n = 12). A second study was performed comparing nasal secretions of 13 subjects allergic to house dust mite to 8 controls.
Compared to controls, leukotrienes and ECP were significantly elevated at nearly all time points in and postseason in the allergic group. Whereas IL-1beta was significantly elevated throughout the study period, IL-1ra was significantly decreased from visit 1 to 3. IL-8 showed no increase compared to controls. Data from subjects with perennial allergic rhinitis supported these findings and additionally demonstrated decreased concentrations of IL-8 and myeloperoxidase in secretions compared to controls.
Allergic rhinitis represents a persistent inflammation in terms of an activation of eosinophils and constant upregulation of the proinflammatory cytokine IL-1beta in the pollen season and thereafter. We additionally could demonstrate a dysfunction of the anti-inflammatory capacity, i.e. IL-1ra, a naturally occurring antagonist. Persistent inflammation may furthermore lead to the dysregulation of local cellular immunity by reducing the number and activity of neutrophils on the mucosal surface.

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    • "AR is characterized by a Th2-polarized inflammation. Th2-derived cytokines, such as IL-4 and IL-13, are the main pathogenic factors able to induce, maintain, and amplify the allergic inflammation.12 In addition, a defect of Treg cells characterizes allergic disorders.4 "
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    ABSTRACT: Allergic rhinitis (AR) is characterized by Th2 polarized immune response. Soluble HLA (sHLA) molecules play an immunomodulatory activity. Two different studies evidenced that both patients with seasonal AR (SAR) and patients with perennial AR (PAR) had higher sHLA-G levels than normal controls. The aim of this study was to compare sHLA-G serum levels in SAR and PAR patients, also considering allergen-specific IgE. One hundred sixty-eight AR patients were enrolled, 94 with SAR and 74 with PAR. A group of 116 healthy subjects was considered as control. sHLA-G and allergen-specific IgE serum levels were determined by immunoenzymatic method. SAR patients had significantly higher levels of sHLA-G than PAR patients (p = 0.0194). sHLA-G was moderately related to allergen-specific IgE both in SAR (r = 0.497) and in PAR patients (r = 0.584). The present study provides evidence that sHLA-G serum levels depend on the type of allergy and are related to allergen-specific IgE serum levels. These findings may suggest that sHLA-G could be a biomarker of allergic reaction.
    03/2014; 5(1). DOI:10.2500/ar.2014.5.0076
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    • "Le taux normal se situe dans une fourchette de 2 à 15 μg/l. La mesure de l'ECP sérique n'est guère utilisée dans les maladies allergiques : certes, globalement, les atopiques évolutifs ont un taux significativement supérieur à celui de sujets sains non atopiques [7]. Mais ce taux est augmenté faiblement, et de façon variable dans la rhinite comme dans l'asthme allergique , ou la dermatite atopique, si bien qu'en pratique, il n'a pas d'intérêt diagnostique car il ne se différencie pas, individuellement , du taux constaté chez des enfants n'ayant pas ces pathologies [35]. "
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    ABSTRACT: SCOPE: The eosinophil cationic protein (ECP) is one of the mediators released during eosinophil activation. These cells are effector cells taking part into the Th2-lymphocyte dependent allergic inflammation. Assaying ECP concentrations in blood and sputum may be useful in evaluating allergic inflammation (asthma and rhinitis). This summary considers the value of measuring ECP levels for the diagnosis of various diseases where an eosinophil-mediated tissue inflammation plays a role. CURRENT SITUATION AND SALIENT POINTS: Levels of eosinophil cationic protein have been determined in nasal secretions, sputum, gastric secretions, feces and serum. They are increased during seasonal allergic rhinitis and perennial rhinitis, allergic asthma and atopic dermatitis. They are also increased in various gastro-intestinal disorders, some of which are associated with IgE: eosinophil intestinal diseases (esophagitis, gastro-enteritis and colitis), gastro-intestinal food allergy and intestinal parasitoses. Finally, they are increased in non IgE-dependent disorders: non allergic asthma with aspirin intolerance, respiratory infections, sinonasal polyposis, Churg-Strauss disease and idiopathic hyper-eosinophilia (HES) syndrome. PERSPECTIVES: Assaying serum ECP could help in the diagnosis of several diseases. With parasitic disease the pathogenic progression may be accurately assessed, when serological tests are less indicative. ECP assay may point to non allergic asthma, either Fernand-Widal syndrome or Churg-Strauss disease. As for gastro-intestinal disorders, it indicates an eosinophilic tissue reaction. In the event of isolated hypereosinophilia, ECP assay may clarify whether it is benign or tending towards idiopathic HES. The assay of peroxidase and eosinophil-derived neurotoxin (EDN) should be also considered.
    La Revue de Médecine Interne 10/2006; 27(9):679-83. · 1.07 Impact Factor
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    Allergy 02/1999; 54 Suppl 57(s57):116-23. DOI:10.1111/j.1398-9995.1999.tb04413.x · 6.03 Impact Factor
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