Secretion of proinflammatory eicosanoid-like substances precedes allergen release from pollen grains in the initiation of allergic sensitization

It is commonly believed that allergic sensitization starts when an allergen contacts the surface of an antigen-presenting cell in mucosal or skin epit helia. Most studies dealing with this aspect use allergen extracts as stimu lus. Under natural exposure conditions, however, the bioavailability of all ergen depends on allergen liberation from internal binding sites within the allergen carrier, e.g. pollen grains. In comparing total protein and major allergen release from timothy grass (Phleum pratense L.) pollen freshly co llected on rural meadows or near high-traffic roads, there was a striking d ifference between the pollen, with higher allergen release rates from rural meadow pollen grains. Thus, allergen release does not explain the higher p revalence rates of atopic sensitization and disease observed in many epidem iological studies in children exposed to automobile exhaust. Therefore, oth er possible effecters from pollen grains were investigated. Pollen grains i ncubated in protein-free buffer were found to secrete significant amounts o f eicosanoid-like substances, namely leukotriene (LT) B-4- like and prostag landin E-2-like substances, in a pH-, time- and temperature-dependent fash ion. The highest values of eicosanoid secretion were found in birch, grass and mugwort pollen, while pine (Pinus sylvestris L.) pollen showed only mar ginal eicosanoid-like secretion. Additionally, the release of these substan ces was significantly higher from pollen which had been collected near road s with heavy traffic, indicating a stronger proinflammatory activity of the se pollen grains. In order to investigate the effects of air pollutants, na tive pollen grains were exposed in a dose- and time-dependent fashion in a fluidized bed reactor to traffic-related pollutants, e.g. volatile organic compounds (toluene, m-xylene), leading again to a significant increase in t he secretion of LTB4-like immunoreactivity, in contrast to exposure with su lfur dioxide. This finding opens a new dimension of understanding of the ea rly events in allergic sensitization, indicating that proinflammatory effec ts of the allergen carrier, e.g. the pollen grain itself, can lead to activ ation of the mucosal membrane. These findings might help to also explain th e higher prevalence rates of pollen allergy in areas with high automobile e xhaust emissions. Furthermore, the allergenic 'potency' of various allergen s has to be redefined at the allergen carrier level with regard to differen t stages of allergen and mediator release prior to the contact with the hos t's immune system. Copyright (C) 2001 S. Karger AG. Basel.