9\alpha,11\beta-PGF_{2}, a arostaglandin D_{2} metabolite, as a marker of mast cell activation in Bee venom-allergic patients

Mast cell (MC) mediators, among them prostaglandin D(2) (PGD(2)) and 9α,11β-PGF(2), PGD(2)’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 PGD(2) and 9α,11β-PGF(2) 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 PGD(2) and 9α,11β-PGF(2) 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-PGF(2) in allergen-challenged chambers to 9α,11β-PGF(2) in allergen-free chambers after 15 min of provocation (p = 0.039). Allergen challenge resulted in a significant increase of 9α,11β-PGF(2) 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 PGD(2) concentration between BVA and healthy subjects. No study patient developed adverse reactions during. 9α,11β-PGF(2) 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

9α,11β-PGF2, a Prostaglandin D2 Metabolite, as a Marker of Mast Cell Activation in Bee Venom-Allergic Patients

Mast cell (MC) mediators, among them prostaglandin D(2) (PGD(2)) and 9α,11β-PGF(2), PGD(2)’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 PGD(2) and 9α,11β-PGF(2) 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 PGD(2) and 9α,11β-PGF(2) 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-PGF(2) in allergen-challenged chambers to 9α,11β-PGF(2) in allergen-free chambers after 15 min of provocation (p = 0.039). Allergen challenge resulted in a significant increase of 9α,11β-PGF(2) 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 PGD(2) concentration between BVA and healthy subjects. No study patient developed adverse reactions during. 9α,11β-PGF(2) 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