The cellular response of the human allergic mucosa to natural allergen exposure

Pipkorn, Ulf; Karlsson, Göran; Enerbäck, Lennart

doi:10.1016/0091-6749(88)90143-1

Cited by 153 publications

(89 citation statements)

References 26 publications

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“…In our study, we also found a strong correlation of clinical data (FEV 1 and VAS score) with inflammatory parameters (eosinophils and IL-5 expression) in allergic lower airways, but were unable to demonstrate any correlation between clinical parameters and inflammatory cell numbers in the nose. Some authors (30,31) reported a correlation between the number of eosinophils or mediators released by eosinophils and symptoms after nasal provocation. Usually, no correlation was found (18,32,33).…”

Section: Discussionmentioning

confidence: 99%

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Braunstahl

KleinJan

Overbeek

et al. 2000

Am J Respir Crit Care Med

354

211

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Allergic rhinitis and asthma often coexist and share a genetic background. Pathophysiologic connections between the nose and lungs are still not entirely understood. This study was undertaken to compare allergic inflammation and clinical findings in the upper and lower airways after segmental bronchial provocation (SBP) in nonasthmatic allergic rhinitis patients. Eight nonasthmatic, grass pollen-sensitive patients with allergic rhinitis and eight healthy controls were included. Bronchial biopsies and blood samples were taken before (T 0 ) and 24 h (T 24 ) after SBP. Nasal biopsies were obtained at T 0 , 1 h after SBP (T 1 ), and T 24 . Immunohistochemical staining was performed for eosinophils (BMK13), interleukin (IL)-5, and eotaxin. The number of eosinophils increased in the challenged and unchallenged bronchial mucosa (p Ͻ 0.05) and in the blood (p ϭ 0.03) of atopic subjects at T 24 . We detected an increase of BMK13-positive and eotaxin-positive cells in the nasal lamina propria and enhanced expression of IL-5 in the nasal epithelium of atopic subjects only at T 24 (p Ͻ 0.05). SBP induced nasal and bronchial symptoms as well as reductions in pulmonary and nasal function in the allergic group. No significant changes could be observed in healthy controls. The study shows that SBP in nonasthmatic allergic rhinitis patients results in peripheral blood eosinophilia, and that SBP can induce allergic inflammation in the nose.Epidemiologic (1), pathophysiologic (2, 3), and clinical studies (4, 5) strongly suggest a link between rhinitis and asthma. Asthma and rhinitis, which are considered to be manifestations of the atopic syndrome, often coexist and share a common genetic background. Although several studies have shown that asthma and rhinitis are characterized by a similar inflammatory process (6-9), pathophysiologic interactions between upper and lower airways are not entirely understood. It is clear that the condition of the upper airways definitely influences the lower airways. In allergic rhinitis patients without bronchial hyperreactivity (BHR), signs of allergic inflammation of the lower airways have been found in induced sputum, bronchoalveolar lavage fluid (BALF), and bronchial biopsy specimens (10-13). The nasal-bronchial reflex, an altered breathing pattern, pulmonary aspiration of nasal contents, and increased levels of inflammatory factors in the blood are possible mechanisms for lower airway dysfunction among patients with rhinitis (14). To shed more light on the role of systemic induction in the allergic inflammatory response, we designed a study in which blood samples and nasal and bronchial mucosal biopsy specimens were taken from a group of nonasthmatic allergic rhinitis patients with an isolated grass pollen allergy after segmental bronchial provocation (SBP) at a time other than the grass pollen season. The aim of the study was to compare allergic mucosal inflammation and clinical findings in the upper and lower airways. Eosinophils, major effector cells in allergic inflammation, interleukin (I...

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Section: Discussionmentioning

confidence: 99%

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Braunstahl

KleinJan

Overbeek

et al. 2000

Am J Respir Crit Care Med

354

211

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“…Eosinophilia is a characteristic feature of allergic rhini tis and asthma [1][2][3][4]. The drugs capable of either inhibiting eosinophil infiltration and/or inhibiting their activation (release of leukotrienes C4 and B4, platelet-activating fac tor, Gi, major basic protein, eosinophil cationic protein, eosinophil peroxidase etc.)…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Aeroallergen-lnduced Bronchial Eosinophilia by Azelastine in Guinea Pigs

Chand

Nolan²,

Diamantis³

et al. 1992

Int Arch Allergy Immunol

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The ability of azelastine to influence allergic bronchial eosinophil infiltration in guinea pigs was studied. Aeroallergen challenge of actively sensitized guinea pigs produces eosinophil infiltration in bronchoalveolar lavage fluid collected 20–24 h after aeroallergen exposure. Azelastine and methylprednisolone, administered orally 2 h before challenge, inhibited eosinophilic infiltration yielding the ED₅₀s of 1.55 and 4.48 mg/kg, respectively. WEB-2086, a platelet-activating factor antagonist (3 mg/kg), and theophylline, a phosphodiesterase inhibitor (30 mg/kg), also suppressed allergic bronchial infiltration of eosinophils by 44%. The data obtained in this study demonstrate that azelastine exerts direct bronchial anti-inflammatory activity in guinea pigs.

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“…The importance of mast cells in host defense to helminths and allergic reactions is emphasized by the increased number of these cells seen in the affected tissues. Thus, mast cell hyperplasia occurs in tissues infected with parasitic helminths (2), and allergic rhinitic subjects have increased mast cell numbers in the nasal mucosa (3)(4)(5). Mouse models of allergic rhinitis have been established (6), and increased mast cell numbers have been reported in the airways of sensitized and allergen-challenged mice (7).…”

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confidence: 99%

Chemotactic action of prostaglandin E₂on mouse mast cells acting via the PGE₂receptor 3

Weller

Collington

Hartnell

et al. 2007

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

118

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Mast cells are long-lived cells that are principally recognized for their effector function in helminth infections and allergic reactions. These cells are derived from pluripotential hematopoietic stem cells in the bone marrow that give rise to committed mast cell progenitors in the blood and are recruited to tissues, where they mature. Little is known about the chemotactic signals responsible for recruitment of progenitors and localization of mature mast cells. A mouse model was set up to identify possible mast cell progenitor chemoattractants produced during repeated allergen challenge in vivo. After the final challenge, the nasal mucosa was removed to produce conditioned medium, which was tested in chemotaxis assays against 2-wk murine bone marrow-derived c-kit ؉ mast cells (BMMC). A single peak of chemotactic activity was seen on reverse-phase HPLC with a retention time and electrospray mass spectrum consistent with prostaglandin E 2 (PGE2). This lipid was found to be a highly potent chemoattractant for immature (2-wk) and also mature (10-wk) BMMC in vitro. Fluorescently labeled 2-wk c-kit ؉ BMMC, when injected intravenously, accumulated in response to intradermally injected PGE2. Analysis using TaqMan showed mRNA expression of the PGE2 receptors 3 (EP3) and 4 (EP4) on 2-and 10-wk BMMC. Chemotaxis induced by PGE2 was mimicked by EP3 agonists, blocked by an EP3 receptor antagonist, and partially inhibited by a MAPKK inhibitor. These results show an unexpected function for PGE2 in the chemotaxis of mast cells.allergy ͉ eicosanoids ͉ migration

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The cellular response of the human allergic mucosa to natural allergen exposure

Cited by 153 publications

References 26 publications

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Inhibition of Aeroallergen-lnduced Bronchial Eosinophilia by Azelastine in Guinea Pigs

Chemotactic action of prostaglandin E₂on mouse mast cells acting via the PGE₂receptor 3

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The cellular response of the human allergic mucosa to natural allergen exposure

Cited by 153 publications

References 26 publications

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Inhibition of Aeroallergen-lnduced Bronchial Eosinophilia by Azelastine in Guinea Pigs

Chemotactic action of prostaglandin E2on mouse mast cells acting via the PGE2receptor 3

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Chemotactic action of prostaglandin E₂on mouse mast cells acting via the PGE₂receptor 3