RGD Reference Report - Regulation of proinflammatory cytokines in seasonal allergic rhinitis. - Rat Genome Database

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Regulation of proinflammatory cytokines in seasonal allergic rhinitis.

Authors: Bachert, C  Van Kempen, M  Van Cauwenberge, P 
Citation: Bachert C, etal., Int Arch Allergy Immunol. 1999 Feb-Apr;118(2-4):375-9.
RGD ID: 4143227
Pubmed: PMID:10224452   (View Abstract at PubMed)
DOI: DOI:24141   (Journal Full-text)

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
rhinitis  IEP 4143227associated with Hypersensitivity and protein:increased expression:nasal mucus RGD 
rhinitis  IEP 4143227associated with HypersensitivityRGD 
rhinitis  ISOIL1B (Homo sapiens)4143227; 4143227associated with Hypersensitivity and protein:increased expression:nasal mucus RGD 
rhinitis  ISOIL1RN (Homo sapiens)4143227; 4143227associated with HypersensitivityRGD 

Objects Annotated

Genes (Rattus norvegicus)
Il1b  (interleukin 1 beta)
Il1rn  (interleukin 1 receptor antagonist)

Genes (Mus musculus)
Il1b  (interleukin 1 beta)
Il1rn  (interleukin 1 receptor antagonist)

Genes (Homo sapiens)
IL1B  (interleukin 1 beta)
IL1RN  (interleukin 1 receptor antagonist)


Additional Information