Background Medicinal remedies of plant origin became very popular in recent
years, and allergic reactions to these are on the rise, accordingly. Camom
ile has been reported as a potential trigger of severe anaphylaxis. The all
ergens responsible for camomile allergy have not been characterized as yet.
Objective The present study aims at reviewing the clinical symptomatology o
f immediate-type reactions in a series of patients sensitized to camomile a
nd at characterizing the responsible allergens.
Methods Fourteen patients with a history of allergy either to camomile or t
o spices or weeds, and a positive skin prick test/RAST to camomile were inv
estigated for related allergic reactions to food, pollen and others. IgE-bi
nding patterns were determined by immunoblotting, inhibition tests and degl
ycosylation experiments.
Results Ten of 14 patients had a clinical history of immediate-type reactio
ns to camomile, in some cases life threatening. Eleven subjects were also s
ensitized to mugwort in prick or RAST, eight to birch tree pollen. Using a
polyclonal rabbit anti-Bet v 1 antibody, a homologue of the major birch pol
len allergen Bet v 1 was detected in two camomile blots. In four cases a gr
oup of higher molecular weight allergens (23-50 kDa) showed IgE-binding to
camomile. All allergens proved heat stable. Binding was inhibited in variab
le degrees by extracts from celery roots, anize seeds and pollen from mugwo
rt, birch and timothy grass. Deglycosylation experiments proved the presenc
e of carbohydrate determinants in camomile which were not responsible for I
gE-binding, though. Profilins (Bet v 2) were not detected in our camomile e
xtracts.
Conclusion Incidence and risk of type I allergy to camomile may be underest
imated. Concurrent sensitization to mugwort and birch pollen is not infrequ
ent. Bet v 1 and noncarbohydrate higher molecular weight proteins were foun
d to be eliciting allergens and are responsible for cross-reactivity with o
ther foods and pollen.