TY - JOUR
T1 - Organic extracts of urban aerosol (≤PM2.5) enhance rBet v 1-induced upregulation of CD63 in basophils from birch pollen-allergic individuals
AU - Schober, Wolfgang
AU - Belloni, Benedetta
AU - Lubitz, Stefanie
AU - Eberlein-König, Bernadette
AU - Bohn, Patrick
AU - Saritas, Yücel
AU - Lintelmann, Jutta
AU - Matuschek, Georg
AU - Behrendt, Heidrun
AU - Buters, Jeroen
PY - 2006/4
Y1 - 2006/4
N2 - Epidemiological studies have linked the high prevalence rates of IgE-mediated allergic diseases to an increase in exposure to traffic-related air pollutants such as diesel exhaust particles (DEPs). There is growing experimental evidence that organic compounds of DEPs, predominantly polycyclic aromatic hydrocarbons (PAHs), participate in the development and maintenance of allergic airway diseases. In this study we investigated the impact of organic extracts of urban aerosol (AERex) containing various PAH concentrations on the activation of human basophils. Whole blood samples from six birch pollen-allergic and five control subjects were repeatedly incubated in the presence of AERex with or without recombinant Bet v 1 (rBet v 1). Basophils were analyzed for CD63 expression as a measure of basophil activation by using multiparameter flow cytometry. Basophils, when exposed in vitro to AERex and rBet v 1, expressed CD63 significantly more than with antigen activation alone. AERex synergized with rBet v 1 in a dose-dependent manner, but did not activate basophils from nonallergic donors. AERex effect on CD63 upregulation was found in blood samples of all patients and did not occur in the absence of rBet v 1. Strongest basophil activation was monitored upon stimulation with AERex comprising the highest PAH content. The capability of AERex to increase activation of basophils from birch pollen-allergic subjects at ambient concentrations suggests an important role of organic compounds of airborne particles in the aggravation of IgE-mediated allergic diseases. This could be a new aspect of regulation of unspecific promoting stimuli in clinical manifestation of allergic inflammation.
AB - Epidemiological studies have linked the high prevalence rates of IgE-mediated allergic diseases to an increase in exposure to traffic-related air pollutants such as diesel exhaust particles (DEPs). There is growing experimental evidence that organic compounds of DEPs, predominantly polycyclic aromatic hydrocarbons (PAHs), participate in the development and maintenance of allergic airway diseases. In this study we investigated the impact of organic extracts of urban aerosol (AERex) containing various PAH concentrations on the activation of human basophils. Whole blood samples from six birch pollen-allergic and five control subjects were repeatedly incubated in the presence of AERex with or without recombinant Bet v 1 (rBet v 1). Basophils were analyzed for CD63 expression as a measure of basophil activation by using multiparameter flow cytometry. Basophils, when exposed in vitro to AERex and rBet v 1, expressed CD63 significantly more than with antigen activation alone. AERex synergized with rBet v 1 in a dose-dependent manner, but did not activate basophils from nonallergic donors. AERex effect on CD63 upregulation was found in blood samples of all patients and did not occur in the absence of rBet v 1. Strongest basophil activation was monitored upon stimulation with AERex comprising the highest PAH content. The capability of AERex to increase activation of basophils from birch pollen-allergic subjects at ambient concentrations suggests an important role of organic compounds of airborne particles in the aggravation of IgE-mediated allergic diseases. This could be a new aspect of regulation of unspecific promoting stimuli in clinical manifestation of allergic inflammation.
KW - Basophils
KW - CD63 expression
KW - Organic compounds of urban aerosol
KW - PM2.5, IgE-mediated allergic diseases
UR - http://www.scopus.com/inward/record.url?scp=33645129085&partnerID=8YFLogxK
U2 - 10.1093/toxsci/kfj092
DO - 10.1093/toxsci/kfj092
M3 - Article
C2 - 16431848
AN - SCOPUS:33645129085
SN - 1096-6080
VL - 90
SP - 377
EP - 384
JO - Toxicological Sciences
JF - Toxicological Sciences
IS - 2
ER -