Asthma, bronchial hyperreactivity and mediator release in children with birch pollinosis. ECP and EPX levels are not related to bronchial hyperreactivity.
BACKGROUND
Symptoms of allergic asthma are triggered by allergen exposure inducing allergic inflammation and hyperreactivity of the bronchi.


OBJECTIVE
To investigate the possible relationship between clinical symptoms and signs of asthma, i.e. bronchial variability as measured by peak expiatory flow rate (PEFR), bronchial hyperreactivity (BHR) and mediators of allergic inflammation.


METHODS
Twenty-eight children with pollinosis, but no obvious history of asthma, were studied at three occasions, i.e. before, during and after (autumn) the birch pollen season. Twelve children sensitive to birch pollen were considered as the case group. Sixteen children, who were only clinically sensitive to grass pollen, served as controls. Subjective symptoms of asthma were recorded by visual analogue scale, BHR was estimated by methacholine bronchial provocation tests, bronchial variability PEFR and circulating mediators of inflammation, i.e. eosinophil cationic protein, eosinophil protein X, myeloperoxidase and tryptase in serum.


RESULTS
Bronchial hyperreactivity and by PEFR was more pronounced after than during the season (P < 0.01), whereas eosinophil mediators and the peak expiratory flow rate increased during the season (P < 0.05). Except for between PEFR variability and BHR in the autumn (r = 0.45; P = 0.014), no correlations were found. However, in the autumn, the majority of children were still hyperreactive in the bronchi and showed PEFR variability but the levels of eosinophil mediators in serum had returned to normal levels.


CONCLUSIONS
Signs and symptoms of asthma did not correlate with serum levels of mediators of allergic inflammation. Bronchial hyperreactivity and PEFR variability persisted after the pollen season when signs of bronchial inflammation had disappeared. We hypothesize that eosinophil mediators and other markers of allergic inflammation disappear after the late-phase reaction, whereas BHR persists. This would explain the lack of correlation between the levels of eosinophil mediators in serum and symptoms of asthma and BHR.
Ferdousi
H A
HA
Department of Paediatrics, University Hospital of Linköping, Sweden.
Dreborg
S
S
D000293:Adolescent; D001249:Asthma / Q000097:blood / Q000276:immunology* / Q000503:physiopathology*; D001798:Blood Proteins / Q000032:analysis* / Q000276:immunology; D016535:Bronchial Hyperreactivity / Q000276:immunology*; D001985:Bronchial Provocation Tests; D002648:Child; D053818:Chymases; D003228:Conjunctiva / Q000276:immunology; D047091:Eosinophil Granule Proteins; D047208:Eosinophil-Derived Neurotoxin; D005260:Female; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D008297:Male; D016210:Methacholine Chloride / Q000494:pharmacology; D010366:Peak Expiratory Flow Rate; D009195:Peroxidase / Q000032:analysis / Q000097:blood; D011058:Pollen / Q000276:immunology; D012260:Ribonucleases; D012621:Seasons; D012697:Serine Endopeptidases / Q000032:analysis / Q000097:blood; D012882:Skin Tests; D014197:Trees / Q000276:immunology; D053802:Tryptases
D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D016210:Methacholine Chloride; D009195:Peroxidase; D047208:Eosinophil-Derived Neurotoxin; D012260:Ribonucleases; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; D053802:Tryptases