Asthma, Rhinitis, Other Respiratory Diseases
Nasal allergen provocation induces adhesion molecule expression and tissue eosinophilia in upper and lower airways,☆☆

https://doi.org/10.1067/mai.2001.113046Get rights and content

Abstract

Background: Allergic rhinitis (AR) and asthma are characterized by means of a similar inflammatory process in which eosinophils are important effector cells. The migration of eosinophils from the blood into the tissues is dependent on adhesion molecules. Objective: To analyze the aspects of nasobronchial cross-talk, we studied the expression of adhesion molecules in nasal and bronchial mucosa after nasal allergen provocation (NP). Methods: Nine nonasthmatic subjects with seasonal AR and 9 healthy control subjects underwent NP out of season. Bronchial and nasal biopsy specimens were taken before (T0) and 24 hours after NP (T24). Mucosal sections were analyzed for the presence of eosinophils, IL-5, eotaxin, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), E-selectin, and human endothelium (CD31). Results: At T24, an influx of eosinophils was detected in nasal epithelium (P = .01) and lamina propria (P < .01), as well as in bronchial epithelium (P = .05) and lamina propria (P < .05), of the patients with AR. At T24, increased expression of ICAM-1, as well as increased percentages of ICAM-1+, VCAM-1+, and E-selectin+ vessels, were seen in nasal and bronchial tissue of patients with AR. The number of mucosal eosinophils correlated with the local expression of ICAM-1, E-selectin, and VCAM-1 in patients with AR. Conclusion: This study shows that NP in patients with AR results in generalized airway inflammation through upregulation of adhesion molecules. (J Allergy Clin Immunol 2001;107:469-76.)

Section snippets

Subject groups

Nine patients with AR (4 men and 5 women; age range, 22-34 years) and 9 nonallergic healthy control subjects (7 men and 2 women; age range, 19-32 years) were selected for the study. Subject characteristics are shown in Table I.

. Subject characteristics

PatientAge (y)SexFEV1 (L)FEV1 (%)IVC (L)FEV1/VCBAR* (%)PC20 (mg/mL)
Patients with AR
  122F3.931084.728810340
  234M3.20873.65889840
  326M4.37955.677710440
  425M4.511014.919210540
  522F3.821124.069410040
  626F3.28934.287710438.4
  722M4.26905.198210719.6
  826F4.72126

Clinical data

At baseline, patients with AR and control subjects were comparable for clinical parameters. At the consecutive 2-hour intervals after NP, the patients with AR had increased total nasal VAS score (P = .0002, repeated-measurement ANOVA) and lower PNIF values (P = .0001) than control subjects. The shape of the nasal VAS score (Fig 2, A ) and PNIF (Fig 2, B ) curves in patients with AR was bimodal, with peaks at T1/2 and T12.

. Symptoms were individually expressed in millimeters on a 10-cm VAS, and a

Discussion

In the current study we were able to show increased expression of endothelial adhesion molecules and eosinophilic allergic inflammation in the nasal and bronchial mucosa of nonasthmatic patients with AR after NP. Recently, we have demonstrated that segmental bronchial provocation in patients with AR induces blood eosinophilia and mucosal inflammation characterized by increased numbers of eosinophils, IL-5+ cells, and eotaxin-positive cells in both upper and lower airways.20 The current study

Acknowledgements

We thank the Allergology Department, the Lung Function Laboratory, the Clinical Chemistry Laboratory, and co-workers of the Pulmonary and E.N.T. research departments, especially Karolina Leman, of the Erasmus University Medical Center Rotterdam for their valuable participation in this study and Sandra Reynhart for editing the manuscript.

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    Supported by a grant from the Dutch Asthma Foundation, Leusden, the Netherlands.

    ☆☆

    Reprint requests: Gert-Jan Braunstahl, MD, Department of Pulmonary Medicine, H-Ee-22.63, EMCR, Dr. Molewaterplein 50, 3015 GE Rotterdam, the Netherlands.

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