Priming of eosinophil adhesion in patients with birch pollen allergy during pollen season: Effect of immunotherapy,☆☆,,★★

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Abstract

The adhesion of eosinophil granulocytes to E-selectin, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) was investigated before and during birch pollen season in 24 patients allergic to birch pollen who had rhinoconjunctivitis and, in half of the cases, asthma during season. Half of the patients were undergoing specific immunotherapy for birch pollen allergy. Increased adhesion to VCAM-1 and ICAM-1 (p < 0.05) during season as compared with before season was demonstrated by eosinophils of patients in the control group and by eosinophils of the patients without asthma treated with immunotherapy, but not by eosinophils from the immunotherapy-treated patients with asthma. Eosinophils from the control group of patients demonstrated increased cell surface expression of CD18 and CD49d (p < 0.05 and p < 0.01, respectively) during season as compared with before season, and eosinophils from the immunotherapy-treated patients showed increased cell surface expression of CD49d (p < 0.01) during season. Simultaneous measurement of neutrophil adhesion revealed increased adhesion to E-selectin and ICAM-1 (p < 0.01) during season compared with before season in the immunotherapy-treated group of patients. Neutrophils from the control subjects without asthma showed increased adhesion to E-selectin (p < 0.05) during season. In conclusion, eosinophils from patients allergic to birch pollen demonstrated priming of the adhesion to VCAM-1 and ICAM-1 during birch pollen season. Immunotherapy treatment prevented the priming of eosinophil adhesion during pollen season in the patients allergic to birch pollen who had asthma, but not in those without asthma. In contrast, neutrophils from the immunotherapy-treated patients, both with and without asthma, demonstrated priming of the adhesion to E-selectin and ICAM-1 during season. The latter results indicate that immunotherapy, in case of the patients allergic to birch pollen with asthma induced a shift from the production of primarily eosinophil priming agents to primarily neutrophil priming agents, which may be caused by a shift from Th2 to Th1 lymphocytes. (J Allergy Clin Immunol 1997;99:551-62.)

Section snippets

Patients

Twenty-four patients allergic to birch pollen participated in the study. There were 11 men and 13 women with a mean age of 31 years (range 21 to 42 years). They all had a history of rhinoconjunctivitis during birch pollen season, and 11 of 24 also had a history of asthma during birch pollen season. The diagnosis of allergy was based on positive results on a skin prick test of >3 mm with birch pollen extract (Betula verrucosa, ALK, Hörsholm, Denmark) and RAST. Some patients were sensitized to

Lung function and blood cell counts

Lung function estimated as FEV1 and PEF values and the bronchial reactivity in the patients measured as PC20 of methacholine before and during season are demonstrated in Table I.

. Lung function in patients before and during birch pollen season and in healthy subjects

GroupFEV1 (%)PEF (%)PC20 methacholine (mg/ml)
Control subjects (n = 12)
 Preseason105 (78-122)102 (80-132)>16 (0.05->16)
 Season94 (69-107)*99 (66-120)*0.74 (0.12->16)*
IT patients (n = 12)
 Preseason97 (80-122)108 (94-132)10.7 (0.09->16)
 

Discussion

The present investigation of eosinophil adhesion in patients allergic to birch pollen was done during the pollen season of 1993, which was a season with extremely high birch pollen counts preceded by high alder pollen counts. The peak mean birch pollen count was about 6000 per cubic meter, whereas the peak count of a “normal” high season in the same area is about 2000 per cubic meter.8, 30 This strong allergen challenge resulted in a significant increase of the bronchial reactivity to

Acknowledgements

The skillful technical assistance of Ms. Annika Svanström and Ms. Agneta Breitholtz is greatly appreciated. We are grateful to Drs. E. Björnsson and C. Janson of the Department of Lung Medicine for allowing us to use some of the reference subjects from the European Community Respiratory Health Survey material.

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  • Cited by (0)

    From the Department of Clinical Chemistrya and the Asthma Research Center,b University Hospital, Uppsala; Department of Otolaryngology,c Central Hospital, Västerås; and Department of Lung Medicine,d Sahlgrenska Hospital, Gothenburg, Sweden.

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    Supported by grants from the Medical Faculty of the University of Uppsala, Bror Herpstedts Stiftelse, the National Association against Asthma and Allergy, and the Swedish Medical Research Council.

    Reprint requests: Lena Håkansson, PhD, Laboratory for Inflammation Research, Department of Clinical Chemistry, University Hospital, S-751 85 Uppsala, Sweden.

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