Increase in IL-8, IL-10, IL-13, and RANTES mRNA levels (in situ hybridization) in the nasal mucosa after nasal allergen provocation

KleinJan, Alex; Dijkstra, M.; Boksa, Simone S.; Severijnen, Lies‐Anne; Mulder, Paul; Fokkens, Wytske J.

doi:10.1016/s0091-6749(99)70469-0

Cited by 89 publications

(62 citation statements)

References 48 publications

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“…The present data suggest that the maturation of IgE-expressing Bcells (activated or memory) to IgE-producing plasma cells takes places in the nose. It is noteworthy that many of the cytokines induced by allergen provocation such as IL-4, IL-6 and IL-13 are also B-cell proliferation factors [11,12,29]. The nasal mucosa might also be the place of maturation of B-cells.…”

Section: Discussionmentioning

confidence: 99%

Local production and detection of (specific) IgE in nasal B-cells and plasma cells of allergic rhinitis patients

et al. 2000

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Allergic diseases are characterized by allergic complaints in the shock organ and specific immunoglobulin (Ig)E in serum. Literature data indicate that the nasal mucosa itself could produce at least a large part of the specific IgE in allergic rhinitis patients.In order to investigate this hypothesis, nasal mucosal biopsies from the inferior turbinate were taken from symptomatic grass pollen allergic rhinitis patients, symptomatic house dust mite allergic rhinitis patients and nonallergic healthy controls, confirmed by radioallergosorbent test and skin-prick test. Immunohistochemical double-staining was performed for B-cells (CD19) with IgE, plasma cells (CD138) with IgE and plasma cells with biotinylated allergens.Significantly more IgE-positive B-cells and IgE-positive plasma cells were found in the nasal mucosa of allergic patients than in that of nonallergic controls. Double staining with biotinylated allergens and plasma cells showed allergen-positive plasma cells in the nasal mucosa of allergic patients and no allergen-positive plasma cells in the nasal mucosa of nonallergic patients. Blocking experiments using polyclonal antibodies directed against IgE showed a significant reduction in the number of allergenpositive cells in contrast to experiments using polyclonal antibodies directed against IgG, IgA or IgM.This study describes new evidence that specific immunoglobulin E is produced locally in the nasal mucosa in patients with seasonal allergic rhinitis and perennial allergic rhinitis, but not in nonallergic controls. Eur Respir J 2000; 15: 491±497.

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Section: Discussionmentioning

confidence: 99%

Local production and detection of (specific) IgE in nasal B-cells and plasma cells of allergic rhinitis patients

et al. 2000

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“…The demonstration of IL-13 expression in eosinophils associated with several allergic, infectious, and idiopathic eosinophilic diseases, however, is a new finding. It is possible that the previously observed correlations between eosinophil number and IL-13 mRNA expression in asthmatic airways (33,34) were largely due to the production of IL-13 by eosinophils themselves.…”

Section: Figure 2 Eosinophils From Eosinophilic Patients Express Il-mentioning

confidence: 99%

Eosinophils Express Functional IL-13 in Eosinophilic Inflammatory Diseases

Schmid‐Grendelmeier

Altznauer

Fischer³

et al. 2002

The Journal of Immunology

216

151

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IL-13 is an immunoregulatory and effector cytokine in allergic diseases such as bronchial asthma. A variety of immune and non-immune cells are known as IL-13 producers. In this study we investigated whether and under what conditions human eosinophils generate IL-13. Freshly isolated highly purified peripheral blood eosinophils from patients with several eosinophilic inflammatory diseases and from normal control individuals were investigated. We observed that blood eosinophils from patients suffering from bronchial asthma, atopic dermatitis, parasitic infections, hypereosinophilic syndrome, and idiopathic eosinophilic esophagitis expressed IL-13, as assessed by ELISA, ELISPOT assay, flow cytometry, and immunocytochemistry. By using nasal polyp tissues and immunohistochemistry, we demonstrated IL-13 expression in eosinophils under in vivo conditions. In contrast, blood eosinophils from control individuals as well as blood neutrophils from both eosinophilic and control patients did not produce detectable IL-13 levels. However, when blood eosinophils from control individuals were stimulated with GM-CSF or IL-5 in vitro, they generated IL-13 mRNA and protein, suggesting that IL-13 expression by eosinophils under inflammatory conditions is a cytokine-driven process. Stimulation of blood eosinophils containing IL-13 by eotaxin resulted in a rapid release of this cytokine. Eosinophil-derived IL-13 was functional, as it increased the surface expression of the low affinity IgE receptor (CD23) on purified B cells. In conclusion, human eosinophils are able to produce and release functional IL-13 in eosinophilic inflammatory responses.

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“…CCL11/eotaxin [6]), is broadly accepted as critical to the eosinophil response. However, CXCL8/interleukin (IL)-8 is also strongly expressed within allergic lesions [7][8][9][10] and eosinophils are responsive to this CXCR1/CXCR2 ligand [11,12]. Indeed, the decreased eosinophilia after allergen immunotherapy may be related to reduced CXCL8/IL-8 responses to allergen challenge [13].…”

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confidence: 99%

Regular salbutamol use increases CXCL8 responses in asthma: relationship to the eosinophil response

Gordon

Swystun²,

Li³

et al. 2003

Eur Respir J

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Regular salbutamol use can exacerbate allergen-induced airway eosinophilia in asthmatics, but its effect on airway eosinophil chemokine responses is unknown.Asthmatic subjects (n=14) were treated for 10 days with placebo or salbutamol in a double-blind, cross-over study, then given same-dose allergen challenges. Their sputa were then analysed 1 and 7 h later for a panel of eosinophil-related cytokines. Eosinophils from five test and three control subjects were tested for expression of CXCL8/interleukin (IL)-8, and its receptors and responsiveness to CCL11/eotaxin and CXCL8/IL-8.Sputum CXCL8/IL-8, but not IL-5, CCL5/regulated on activation, T-cell expressed and secreted, CCL7/monocyte chemotactic protein-3, CCL11/eotaxin, granulocytemacrophage colony-stimulating factor or tumour necrosis factor levels, were increased (42%) by the salbutamol treatments. The CXCL8/IL-8 levels correlated with the proportions of sputum eosinophils and these cells, but not other sputum cells, stained strongly for CXCL8/IL-8. The circulating eosinophils of the tested subjects (n=5) expressed CXCL8/IL-8 receptors and secreted high levels of this chemokine. Neutralisation of sputum CXCL8/IL-8 reduced eosinophil chemotactic responses to these samples by 19¡5%.These data suggest that regular use of salbutamol can augment airway CXCL8/ interleukin-8 responses to allergen challenge and that this CXCL8/interleukin-8 could contribute to the airway inflammatory response. Eur Respir J 2003; 22: 118-126 Inhaled b 2 -adrenergic receptor agonists (b 2 -agonists) comprise a primary therapy for bronchoconstriction in allergic asthma patients. However, evidence suggests that regular use of b 2 -agonists can reduce their effectiveness [1, 2] and lead to increased airway hyperresponsiveness [3][4][5] and eosinophil/ mast cell responses [4,5] to allergen challenge. Given the association of eosinophils with asthma severity and pathology [6], the cellular mechanisms that may regulate this eosinophil response were questioned.Eosinophils express receptors for many molecules that are highly pertinent to asthma pathophysiology [6]. For example, the CCR3 receptor, which binds multiple CC chemokines (e.g. CCL11/eotaxin [6]), is broadly accepted as critical to the eosinophil response. However, CXCL8/interleukin (IL)-8 is also strongly expressed within allergic lesions [7][8][9][10] and eosinophils are responsive to this CXCR1/CXCR2 ligand [11,12]. Indeed, the decreased eosinophilia after allergen immunotherapy may be related to reduced CXCL8/IL-8 responses to allergen challenge [13].In a recent study in which mildly asthmatic subjects (n=14) regularly used salbutamol (or placebo) for 10 days, an exacerbation of asthmatic responses (forced expiratory volume in one second (FEV1), serum tryptase and sputum eosinophils) to allergen challenge was observed [5]. In order to gain insight into potential mechanisms behind this eosinophilia [4,5], a panel of nine pertinent eosinophil-signalling cytokines/ chemokines in sputum, previously obtained from these subjec...

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Increase in IL-8, IL-10, IL-13, and RANTES mRNA levels (in situ hybridization) in the nasal mucosa after nasal allergen provocation

Cited by 89 publications

References 48 publications

Local production and detection of (specific) IgE in nasal B-cells and plasma cells of allergic rhinitis patients

Local production and detection of (specific) IgE in nasal B-cells and plasma cells of allergic rhinitis patients

Eosinophils Express Functional IL-13 in Eosinophilic Inflammatory Diseases

Regular salbutamol use increases CXCL8 responses in asthma: relationship to the eosinophil response

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