Dynamics of nasal eosinophils in response to a nonnatural allergen challenge in patients with allergic rhinitis and control subjects: A biopsy and brush study1

Godthelp, Tom; Holm, Adriaan; Fokkens, Wytske J.; Doornenbal, Peter; Mulder, Paul; Hoefsmit, E. C. M.; KleinJan, Alex; Prens, Errol P.; Rijntjes, E.

doi:10.1016/s0091-6749(96)80158-8

Cited by 57 publications

(42 citation statements)

References 30 publications

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“…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%

“…Staining for eosinophils with BMK13 was done with a modified alkaline phosphatase (AP) method (18). (IL)-5 and eotaxin staining were done as follows: briefly, each tissue specimen was cut into serial, 6-m-thick sections on a Reichert-Jung 2800e Frigocut cryostat (Leica, Wetzlar, Germany) and transferred onto poly-L -lysine-coated slides (Sigma Chemical Co., St. Louis, MO), dried, and stored at Ϫ 70 Њ C. The slides were stained within 3 mo.…”

Section: Immunohistochemical Stainingmentioning

confidence: 99%

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Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Braunstahl

KleinJan

Overbeek

et al. 2000

Am J Respir Crit Care Med

357

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%

Section: Immunohistochemical Stainingmentioning

confidence: 99%

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Braunstahl

KleinJan

Overbeek

et al. 2000

Am J Respir Crit Care Med

357

211

View full text Add to dashboard Cite

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“…In studies of individuals with asthma, [33][34][35] allergic rhinitis, 36,37 and nasal polyposis, 13,38,39 approximately 67% of all airway mucosal eosinophils were shown to exhibit intact but lucent granules indicative of PMD. In allergenexposed nasal airways, virtually all viable eosinophils in mucosal tissue showed signs of PMD under active disease conditions.…”

Section: Discussionmentioning

confidence: 99%

Translocation of the tetraspanin CD63 in association with human eosinophil mediator release

Mahmudi‐Azer

Downey

Moqbel

2002

Blood

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The tetraspanin CD63 (also known as LAMP-3) has been implicated in phagocytic and intracellular lysosome-phagosome fusion events. It is also present in eosinophils, with predominant expression on crystalloid granule membrane. However, its role in eosinophil function is obscure. We hypothesized that CD63 is associated with intracellular events involved in eosinophil activation and mediator release. We used a combination of confocal immunofluorescence microscopy, flow cytometry, and secretion assays, including ␤-hexosaminidase, eosinophil peroxidase, and RANTES, to examine CD63 expression, intracellular localization, and its association with cell activation and mediator release. In resting eosinophils, CD63 immunoreactivity was localized to plasma and crystalloid granule membranes. In interferon-␥ (IFN-␥)-or C5a/CB-stimulated cells (10 minutes), intracellular CD63 appeared to shift to the cell periphery and plasma membrane, while stimulation with a cocktail of interleukin-3 (IL-3)/IL-5/granulocyte-macrophage colony-stimulating factor induced the appearance of discrete intracellular clusters of CD63 immunoreactivity. IFN-␥ induced mobilization of CD63 to the cell periphery, which coincided with selective mobilization of RANTES prior to its release, implying CD63 association with piecemeal degranulation. Agonist-induced CD63 mobilization and cell surface upregulation was associated with ␤-hexosaminidase, eosinophil peroxidase, and RANTES release. Dexamethasone as well as genistein (a broad-spectrum inhibitor of tyrosine kinases) inhibited agonistinduced intracellular mobilization of CD63 and RANTES together with cell surface up-regulation of CD63 and mediator release. This is the first report of an association between CD63 mobilization and agonist-induced selective mediator release, which may imply the involvement of CD63 in eosinophil activation and piecemeal degranulation. IntroductionEosinophils are major effector cells in allergic inflammation and asthma. 1-3 They synthesize, store, and release a wide range of proinflammatory mediators, including at least 4 cationic proteins 1,2 and up to 23 cytokines and growth factors. 4,5 Eosinophils contain different populations of mediator-storage organelles, including small secretory vesicles as well as crystalloid granules. The latter secretory granules are the site of storage of cytotoxic cationic proteins as well as a number of cytokines, chemokines, and growth factors. 6,7 The membrane-bound crystalloid granule comprises 2 compartments: an electron-dense crystalline core (internum) where major basic protein (MBP) 8,9 is stored and an electron-lucent matrix 6 where 3 cationic proteins-namely, eosinophil cationic protein, eosinophil peroxidase (EPO), and eosinophil-derived neurotoxin 1,8 -together with a number of other cytokines, including interleukin-6 (IL-6) 10 and RANTES (regulated on activation normal T cells expressed and secreted), 11 are stored. Among eosinophilderived mediators, ␤-hexosaminidase (␤-hex) has been shown to localize to both small secretory vesicle...

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“…Nasal biopsies provide more reproducible information than nasal brushings on the nasal epithelium and the musosa, and additionally on the submucosa as well, however, the methodology does not allow frequently repeated samplings within one individual [190].…”

Section: Overview Of Sampling Techniquesmentioning

confidence: 99%

Biomarkers in asthma and allergic rhinitis

Diamant

Boot

Mantzouranis

et al. 2010

Pulmonary Pharmacology & Therapeutics

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Dynamics of nasal eosinophils in response to a nonnatural allergen challenge in patients with allergic rhinitis and control subjects: A biopsy and brush study1

Abstract: CLIN IMMUNOL 1996;97:800-11.)

Cited by 57 publications

References 30 publications

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Translocation of the tetraspanin CD63 in association with human eosinophil mediator release

Biomarkers in asthma and allergic rhinitis

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