Abstract
Mast cell (MC) mediators, among them prostaglandin D2 (PGD2) and 9α,11β-PGF2, PGD2’s metabolite, play a key role in allergic reactions, including bee venom anaphylaxis (BVA). Assessment of these mediators has never been performed in BVA. The aim of the study was to assess the activation of MC during in vivo provocation with bee venom (BV) and to measure PGD2 and 9α,11β-PGF2 in the course of an allergen challenge. The second aim was to determine if assessment of these mediators could be useful for predicting adverse events during venom immunotherapy (VIT). In 16 BV-VIT patients and 12 healthy subjects, levels of PGD2 and 9α,11β-PGF2 were assessed during BV provocation by means of the skin chamber method. Chamber fluids, collected at 5 and 15 min, were analyzed for both mediators by gas chromatography mass spectrometry negative ion chemical ionization. BVA in comparison to non-allergic patients had a significantly higher ratio of 9α,11β-PGF2 in allergen-challenged chambers to 9α,11β-PGF2 in allergen-free chambers after 15 min of provocation (p = 0.039). Allergen challenge resulted in a significant increase of 9α,11β-PGF2 levels between 5 and 15 min after provocation only in BVA patients (p < 0.05). Analysis of log-transformed PGD2 levels showed significant difference between changes in PGD2 concentration between BVA and healthy subjects. No study patient developed adverse reactions during. 9α,11β-PGF2 is actively generated during the early allergic response to BV. Skin chamber seems to be a promising, non-invasive and safe model of in vivo allergen provocation in BV-allergic patients. High or low levels of both mediators do not predict occurrence of adverse events during VIT.
Highlights
Severe systemic allergic reactions to bee venom (BV) are potentially life-threatening events, which makes this type of allergy a serious clinical problem (Antonicelli et al 2002; Bilo 2011)
The aim of the study was to assess the activation of Mast cell (MC) during in vivo provocation with bee venom (BV) and to measure prostaglandin D2 (PGD2) and 9a,11b-PGF2 in the course of an allergen challenge
From the point of view of our investigation, especially important are studies assessing the production of PGD2 and its metabolites after provocation with allergens (Sood et al 2013)
Summary
Severe systemic allergic reactions to bee venom (BV) are potentially life-threatening events, which makes this type of allergy a serious clinical problem (Antonicelli et al 2002; Bilo 2011). Specific IgE-based measurements: intradermal tests (IDT) with venom extract and specific serum IgE (sIgE) detected with ultrasensitive immunocapture methods are the main tool in the diagnosis of patients with the history of systemic reactions to bee sting (Tracy et al 2011). These diagnostic tools can neither adequately predict severity of future sting reactions nor serve to monitor clinical reactivity to insect sting. There is still research going on to work out clinically relevant markers of venom anaphylaxis and immunoresponse to venom immunotherapy (VIT). Among in vitro detectable MC-derived mediators, only serum tryptase has an established position in the diagnosis of venom anaphylaxis both in adults and children (Brown et al 2013; Rueff et al 2009)
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