A novel inhalation allergen present in the working environment of beekeepers.

BACKGROUND: Inhalation allergies, caused by allergens from various kinds of pollen, house dust mites, animal epithelium, and mould fungi, are strongly increasing in frequency. In 2.6% of the cases the allergen source remains unidentified. The present paper describes a so far unknown inhalation allergy which was observed in the case of a patient working with hives. METHODS AND RESULTS: The allergen was characterized by immunoblotting, enzyme-linked immunosorbent assay inhibition, and isoelectrofocusing, using the serum of the patient. It is present in both the bee bodies and the larvae, has a molecular mass of 13 kDa, and an isoelectric point of 5.85. It is thermolabile and does not cross-react with allergens from birch, mugwort and timothy grass pollen, mould fungi, or bee venom. The N-terminal amino acid sequence of allergen from larvae was determined to be (2)QIEELKTRLHT(12). A similar allergen of 13 kDa was also found in Varroa mite accompanying bee populations. CONCLUSION: Honey bees (including the larva stadium) and Varroa mite contain a 13-kDa protein causing an allergic reaction. Presently, there is no evidence whether the case described is a singular phenomenon or whether this allergen is a more common inducer of allergies among subjects exposed to honey bees. However, a bee and Varroa mite allergy has to be considered for beekeepers after exclusion of known inhalation allergies.

Effects of tebuconazole on morphology, structure, cell wall components and trichothecene production of Fusarium culmorum in vitro.

The effects of tebuconazole, a systemic fungicide, on the morphology, structure, cell wall components and toxin production of Fusarium culmorum were investigated in vitro. Treatment was by application of four filter paper strips (0.75 cm x 5.0 cm) soaked in 20 micrograms ml-1 fungicide placed around a point inoculum in Petri dishes. Mycelial growth was strongly inhibited by fungicide treatment. Scanning electron microscopic observations showed that the fungicide caused irregular swelling and excessive branching of hyphae. The morphological changes induced by the fungicide at the ultrastructural level included considerable thickening of the hyphal cell walls, excessive septation, the formation of the incomplete septa, extensive vacuolisation, accumulation of lipid bodies and progressing necrosis or degeneration of the hyphal cytoplasm. Non-membrane inclusion bodies were often detected in the hyphal cytoplasm. Furthermore, the formation of new hyphae (daughter hyphae) inside collapsed hyphal cells was common following treatment. The daughter hyphae also displayed severe alterations such as irregular thickening of the cell walls and necrosis of the cytoplasm. Using cytochemical techniques, the labelling densities of chitin and beta-1,3-glucan in the cell walls of the fungicide-treated hyphae were more pronounced than in those of the control hyphae. Moreover, immunogold labelling with antiserum against deoxynivalenol (DON) revealed that Fusarium toxin DON was localized in the cell walls, cytoplasm, mitochondria and vacuoles of the hyphae from the control and the fungicide treatment, but the labelling density in the fungicide-treated hyphae decreased dramatically compared with the control hyphae, indicating that tebuconazole reduced Fusarium toxin production of the fungus.

[Asthma therapy for adults]. / Therapie des Asthma bronchiale im Erwachsenenalter.

The goal of asthma management is to achieve control of the condition. This essentially requires environmental control measures (allergen avoidance) and patient training and education. Drug treatment comprises anti-inflammatory (corticosteroids), and bronchodilatory controller therapy (long-acting beta 2-sympathomimetics, leukotriene receptor antagonists, retarded theophylline) as well as bronchodilatory medication as required (short-acting beta 2-sympathomimetics). The number and frequency of pharmacologic therapy relates to the severity of the clinical presentation. The combination of certain controller drugs (corticosteroids with long-acting beta 2-agonists, corticosteroids with leukotriene receptor antagonists, and beta 2-agonists with leukotriene receptor antagonists) yields a synergistic therapeutic effect as well as a compliance advantage.

Surface membrane antigen alteration on blood basophils in patients with Hymenoptera venom allergy under immunotherapy.

BACKGROUND: Venom immunotherapy (VIT) provides widespread protection against systemic anaphylactic reactions after a sting of the respective insect. This effect is attributed to a shift from T(H)2 to T(H)1. However, because basophils also produce and release cytokines, such as IL-4 and IL-13, they may be part of the cytokine network. The cytokines may regulate basophilic granulocytes, as suggested by the presence of cytokine receptors IL-2Ralpha, GM-CSFRalpha, IL-1RII, IL-3R, IL-4R, IL-5R, and IL-6R on basophils from nonallergic donors. OBJECTIVE: The purpose of this study was to demonstrate that human basophils from subjects allergic to wasp venom undergoing VIT are regulated by cytokines, as shown by the alteration of the expression of cytokine receptors (and other markers). METHODS: The expression of the surface interleukin receptors and activation antigens on basophils from 19 nonallergic subjects and 48 patients with wasp venom allergy was investigated before, immediately after, and 1 week after VIT (20 patients only). RESULTS: Basophilic granulocytes in allergic subjects, compared with those in healthy persons, showed elevated expression of CD32 (FcgammaRII), CD122 (IL-2Rbeta), CD124 (IL-4Ralpha), CD130 (IL-6 and 11Rbeta), CD154 (CD40L), and HLA-DR. Activation of basophils clearly increased during VIT indicated by increased expression of CD32, CD33, CD35 (CR1), CD63, CD116 (GM-CSFRalpha), CD122, CD124, CD130, and CD154. HLA-DR expression also tended to increase. The expression of IL-5R (CD125) decreased. A significant decrease of the basophilic surface antigens CD11c, CD32, CD35, CD63, CD116, CD122, CD124, CD130, and CD132 (interleukin receptor gamma) was detected 1 week after the end of rush VIT. CONCLUSION: The rise in CD63 during VIT indicates a partial basophil degranulation with release of stored protein mediators, including IL-4. IL-4 may cause a transient upregulation of different surface antigens in an autocrine manner. Thereafter, cytokines released by T cells, which as a result of VIT have changed from a T(H)2 type to a more T(H)1 type, downregulate the activation of the basophilic granulocytes.