Nasal eosinophilia and IL-5 mRNA expression in seasonal allergic rhinitis induced by natural allergen exposure: Effect of topical corticosteroids☆☆☆★★★

Masuyama, Keisuke; Till, Stephen J.; Jacobson, Mikila R.; Kamil, A.; Cameron, Lisa; Júlíusson, Sigurður; Löwhagen, O.; Kay, A. B.; Hamid, Qutayba; Durham, Stephen R.

doi:10.1016/s0091-6749(98)70277-5

Cited by 50 publications

(36 citation statements)

References 21 publications

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“…Our results are most suggestive of a general systemic activation of eosinophils, which leads to migration of these cells into both the upper and lower respiratory mucosa. The detection of increased expression of the proeosinophilic cytokines (IL)-5 and granulocyte-macrophage colony-stimulating factor in the serum of allergic rhinitis patients after nasal allergen provocation supports our hypothesis (22). Nasal provocation with methacholine in asthmatic patients with rhinitis resulted in an increase in lower airway resistance that could be blocked by premedication of the nasal mucosa with phenylephrine, also suggesting a role for systemic absorption in the induction of lower airway resistance (23).…”

Section: Discussionsupporting

confidence: 71%

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: Discussionsupporting

confidence: 71%

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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“…Although these data strongly suggest local eosinophil differentiation, they do not in any way exclude a role for eosinophil infiltration. Elevated numbers of peripheral blood (46,47) as well as tissue (27,48) eosinophils in subjects with allergic disorders are well documented. Our present work indicates, however, that, in addition to the infiltration of mature eosinophils, a population may originate from within the target organ itself.…”

Section: Discussionmentioning

confidence: 99%

“…An increased number of IL-5 mRNA ϩ cells is a well recognized characteristic of allergic respiratory mucosa (48,53) and has been considered to be the consequence of inflammatory cell infiltration. Here, we demonstrate the production of IL-5 mRNA following ex vivo stimulation, providing direct evidence that local inflammatory cells increase their cytokine production following allergen exposure.…”

Section: Discussionmentioning

confidence: 99%

Evidence for Local Eosinophil Differentiation Within Allergic Nasal Mucosa: Inhibition with Soluble IL-5 Receptor

Cameron

Christodoulopoulos

Lavigne

et al. 2000

The Journal of Immunology

125

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Eosinophil differentiation occurs within the bone marrow in response to eosinopoietic cytokines, particularly IL-5. Recently, however, eosinophil precursors (CD34/IL-5Rα+ cells) and IL-5 mRNA+ cells have been identified within the lungs of asthmatics, indicating that a population of eosinophils may differentiate in situ. In this report, we examined the presence of eosinophil precursors within allergic nasal mucosa and examined whether they undergo local differentiation following ex vivo stimulation. We cultured human nasal mucosa obtained from individuals with seasonal allergic rhinitis with either specific allergen, recombinant human IL-5 (rhIL-5), or allergen + soluble IL-5Rα (sIL-5Rα), shown to antagonize IL-5 function. Simultaneous immunocytochemistry and in situ hybridization demonstrated that there were fewer cells coexpressing CD34 immunoreactivity and IL-5Rα mRNA following culture with allergen or rhIL-5, compared with medium alone. Immunostaining revealed that the number of major basic protein (MBP) immunoreactive cells (eosinophils) was higher within tissue stimulated with allergen or rhIL-5, compared with unstimulated tissue. In situ hybridization detected an increase in IL-5 mRNA+ cells in sections from tissue cultured with allergen, compared with medium alone. These effects were not observed in tissue cultured with a combination of allergen and sIL-5Rα. Colocalization analysis indicated this expression to be mainly, but not exclusively, T cell (44%) and eosinophil (10%) derived. Our findings suggest that a subset of eosinophils may differentiate locally within allergic nasal mucosa, in what appears to be a highly IL-5-dependent fashion, and imply that this process might be regulated in vivo by endogenous production of sIL-5Rα.

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“…Clinically, little evidence is available with regard to AEP. However, it is well documented that the anti-inflammatory effect of corticosteroids on bronchial asthma and allergic rhinitis is associated with a reduction in topical IL-5 expression [41, 42]. In another study, IL-5 mRNA was expressed in bronchoalveolar cells from patients with chronic cough responsive to inhaled corticosteroids, while it was not detected in unresponsive patients [43].…”

Section: Discussionmentioning

confidence: 99%

Increased Interleukin-5 Levels in Bronchoalveolar Lavage Fluid Is a Major Factor for Eosinophil Accumulation in Acute Eosinophilic Pneumonia

Nakahara

Hayashi²,

Fukuno³

et al. 2001

Respiration

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Background: Increased interleukin-5 (IL-5) levels have been reported in bronchoalveolar lavage fluid (BALF) from patients with acute eosinophilic pneumonia (AEP); however, it still remains to be determined whether IL-5 is responsible for the eosinophil accumulation in the lung. Objective: We examined the effect of antibodies against cytokines on eosinophil chemotaxis induced by BALF from AEP patients to identify factors responsible for eosinophil accumulation. Methods: We measured a series of specific cytokines, including IL-3, IL-4, IL-5, IL-6, IL-8, GM-CSF, RANTES, MCP-1, MIP-1α and eotaxin, in the BALF from 4 patients with AEP. BALF from 4 patients with chronic eosinophilic pneumonia (CEP) and 13 patients with non-eosinophilic interstitial lung diseases (ILD) were examined as controls. The eosinophil chemotactic activity in the BALF was examined using tissue culture insert furnished with a polycarbonate membrane. Results: The total protein content in BALF from patients with AEP was extremely elevated. Even after standardization with protein concentration, IL-5 levels in AEP patients were significantly higher than those in CEP and ILD. IL-3 and chemokines were rather lower in the AEP group than in the CEP and ILD groups. In AEP BALF, anti-IL-5 neutralizing antibody significantly inhibited eosinophil chemotaxis. Antibodies against IL-3, GM-CSF, and IL-8 did not affect the eosinophil migration. Conclusion: These findings suggest that locally produced IL-5 plays an important role in eosinophil accumulation of AEP.

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Nasal eosinophilia and IL-5 mRNA expression in seasonal allergic rhinitis induced by natural allergen exposure: Effect of topical corticosteroids☆☆☆★★★

Cited by 50 publications

References 21 publications

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Evidence for Local Eosinophil Differentiation Within Allergic Nasal Mucosa: Inhibition with Soluble IL-5 Receptor

Increased Interleukin-5 Levels in Bronchoalveolar Lavage Fluid Is a Major Factor for Eosinophil Accumulation in Acute Eosinophilic Pneumonia

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