Nasal provocation with allergen induces a secondary serum IgE antibody response

Naclerio, Robert M.; Adkinson, N. Franklin; Moylan, Birgitta; Baroody, Fuad M.; Kagey‐Sobotka, Anne; Lichtenstein, Lawrence M.; Hamilton, Robert G.

doi:10.1016/s0091-6749(97)70143-x

Cited by 38 publications

(33 citation statements)

References 12 publications

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“…In vivo studies in human subjects have demonstrated that glucocorticoids inhibit the seasonal increase in IgE in the airways and in the serum of allergic individuals (57,58). The prevailing view is that glucocorticoids achieve these effects by inhibiting the production of cytokines such as IL-4 and IL-13 that induce CSR, because B cell responses in vitro are resistant to glucocorticoids.…”

Section: Discussionmentioning

confidence: 99%

Airway Epithelial Cells Produce B Cell-Activating Factor of TNF Family by an IFN-β-Dependent Mechanism

Kato

Truong-Tran

Scott

et al. 2006

The Journal of Immunology

146

114

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Activation of B cells in the airways is now believed to be of great importance in immunity to pathogens, and it participates in the pathogenesis of airway diseases. However, little is known about the mechanisms of local activation of B cells in airway mucosa. We investigated the expression of members of the B cell-activating TNF superfamily (B cell-activating factor of TNF family (BAFF) and a proliferation-inducing ligand (APRIL)) in resting and TLR ligand-treated BEAS-2B cells and primary human bronchial epithelial cells (PBEC). In unstimulated cells, expression of BAFF and APRIL was minimal. However, BAFF mRNA was significantly up-regulated by TLR3 ligand (dsRNA), but not by other TLR ligands, in both BEAS-2B cells (376-fold) and PBEC (224-fold). APRIL mRNA was up-regulated by dsRNA in PBEC (7-fold), but not in BEAS-2B cells. Membrane-bound BAFF protein was detectable after stimulation with dsRNA. Soluble BAFF protein was also induced by dsRNA (>200 pg/ml). The biological activity of the epithelial cell-produced BAFF was verified using a B cell survival assay. BAFF was also strongly induced by IFN-β, a cytokine induced by dsRNA. Induction of BAFF by dsRNA was dependent upon protein synthesis and IFN-αβ receptor-JAK-STAT signaling, as indicated by studies with cycloheximide, the JAK inhibitor I, and small interfering RNA against STAT1 and IFN-αβ receptor 2. These results suggest that BAFF is induced by dsRNA in airway epithelial cells and that the response results via an autocrine pathway involving IFN-β. The production of BAFF and APRIL by epithelial cells may contribute to local accumulation, activation, class switch recombination, and Ig synthesis by B cells in the airways.

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Section: Discussionmentioning

confidence: 99%

Airway Epithelial Cells Produce B Cell-Activating Factor of TNF Family by an IFN-β-Dependent Mechanism

Kato

Truong-Tran

Scott

et al. 2006

The Journal of Immunology

146

114

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“…It is well established that respiratory allergen contact during the pollen season or in the context of nasal allergen exposure induces strong rises of allergen-specific IgE Abs, presumably because of activation of allergen-specific epsilon memory B cells that reside in or in the vicinity of the respiratory tract (5,28,29). The time course of exposure to pollen from birch and trees containing Bet v 1-cross-reactive allergens is displayed in Fig.…”

Section: Vaccinated Patients Show a Reduced Boosting Of Ige Memory Re-mentioning

confidence: 99%

Vaccination with genetically engineered allergens prevents progression of allergic disease

Niederberger

Horak

Vrtala

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

331

316

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IgE-mediated allergy affects >25% of the population in industrialized countries. Repeated contact with the disease-eliciting allergens induces rises of allergen-specific IgE Abs and progression of the disease to more severe manifestations. Our study uses a type of vaccine that is based on genetically modified allergen derivatives to treat allergic patients. We developed hypoallergenic derivatives of the major birch pollen allergen, Bet v 1, by genetic engineering and vaccinated birch pollen-allergic patients (n ‫؍‬ 124) in a double-blind, placebo-controlled study. Active treatment induced protective IgG Abs that inhibited allergen-induced release of inflammatory mediators. We also observed a reduction of cutaneous sensitivity as well as an improvement of symptoms in actively treated patients. Most important, rises of allergen-specific IgE induced by seasonal birch pollen exposure were significantly reduced in vaccinated patients. Vaccination with genetically engineered allergen derivatives is a therapy for allergy that not only ameliorates allergic reactions but also reduces the IgE production underlying the disease.

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“…A group challenged intranasally with Bet v 1 was included as a positive control because it has been shown that intranasal challenge with Bet v 1 induces systemic rises of Bet v 1‐specific IgE levels 20, 21, 22, 23. One subject of the omalizumab group dropped out 1 day before intranasal challenge due to a viral upper respiratory tract infection.…”

Section: Resultsmentioning

confidence: 99%

“…The pilot clinical trial performed by intranasal administration of Bet v 1 and omalizumab was based on the observation that intranasal administration of allergen to allergic patients induced a robust increase in allergen‐specific IgE antibodies, eventually by targeting IgE‐producing cells 20, 21, 22, 23. In fact, histological analyses of nasal mucosal biopsies have revealed the presence of IgE + B cells and plasma cells in the nasal mucosa 18.…”

Section: Discussionmentioning

confidence: 99%

“…In the nasal mucosa of allergic patients, the presence of IgE + B cells as well as plasma cells18 and local IgE production19 have been demonstrated. In addition, a strong rise of systemic allergen‐specific IgE has been observed in subjects after nasal administration of allergens20, 21, 22, 23 indicating the potential presence of memory IgE + B cells in the nasal mucosa. We therefore investigated the effect of intranasal administration of omalizumab, allergen or placebo on allergen‐specific and total systemic IgE.…”

Section: Introductionmentioning

confidence: 99%

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Intranasal administration of allergen increases specific IgE whereas intranasal omalizumab does not increase serum IgE levels—A pilot study

Eckl‐Dorna

Fröschl

Lupinek

et al. 2017

Allergy

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BackgroundAdministration of the therapeutic anti‐IgE antibody omalizumab to patients induces strong increases in IgE antibody levels.ObjectiveTo investigate the effect of intranasal administration of major birch pollen allergen Bet v 1, omalizumab or placebo on the levels of total and allergen‐specific IgE in patients with birch pollen allergy.MethodsBased on the fact that intranasal allergen application induces rises of systemic allergen‐specific IgE, we performed a double‐blind placebo‐controlled pilot trial in which birch pollen allergic subjects were challenged intranasally with omalizumab, placebo or birch pollen allergen Bet v 1. Total and allergen‐specific IgE, IgG and basophil sensitivity were measured before and 8 weeks after challenge. For control purposes, total, allergen‐specific IgE levels and omalizumab‐IgE complexes as well as specific IgG levels were studied in subjects treated subcutaneously with either omalizumab or placebo. Effects of omalizumab on IgE production by IL‐4/anti‐CD40‐treated PBMCs from allergic patients were studied in vitro.ResultsIntranasal challenge with Bet v 1 induced increases in Bet v 1‐specific IgE levels by a median of 59.2%, and this change differed significantly from the other treatment groups (P = .016). No relevant change in allergen‐specific and total IgE levels was observed in subjects challenged with omalizumab. Addition of omalizumab did not enhance IL‐4/anti‐CD40‐induced IgE production in vitro. Significant rises in total IgE (mean IgE before: 131.83 kU/L to mean IgE after: 505.23 kU/L) and the presence of IgE‐omalizumab complexes were observed after subcutaneous administration of omalizumab.ConclusionIntranasal administration of allergen induced rises of allergen‐specific IgE levels, whereas intranasal administration of omalizumab did not enhance systemic total or allergen‐specific IgE levels.

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Nasal provocation with allergen induces a secondary serum IgE antibody response

Cited by 38 publications

References 12 publications

Airway Epithelial Cells Produce B Cell-Activating Factor of TNF Family by an IFN-β-Dependent Mechanism

Airway Epithelial Cells Produce B Cell-Activating Factor of TNF Family by an IFN-β-Dependent Mechanism

Vaccination with genetically engineered allergens prevents progression of allergic disease

Intranasal administration of allergen increases specific IgE whereas intranasal omalizumab does not increase serum IgE levels—A pilot study

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