Bee venom allergy

Annila, Ilkka

doi:10.1046/j.1365-2222.2000.00885.x

Cited by 29 publications

(28 citation statements)

References 70 publications

(76 reference statements)

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“…Venoms also can induce allergic sensitization and development of specific IgE antibodies (Annila, 2000; Charavejasarn et al, 1975; Jarisch et al, 1979; Saelinger and Higginbotham, 1974; Wadee and Rabson, 1987), which bind to the high affinity IgE receptor, FcεRI, on tissue mast cells (MCs) and blood basophils, priming them to release mediators of allergy and anaphylaxis upon subsequent venom exposure (Charavejasarn et al, 1975; Finkelman, 2007; Galli and Tsai, 2012; Oettgen and Geha, 1999; Saelinger and Higginbotham, 1974). MCs also can be activated directly by certain venoms, in the absence of specific IgE, and work in mice indicates that innate functions of MCs, including degradation of venom toxins by MC-derived proteases, can enhance host resistance to the venoms of certain arthropods (including the honeybee) and reptiles (Akahoshi et al, 2011; Metz et al, 2006; Schneider et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

A Beneficial Role for Immunoglobulin E in Host Defense against Honeybee Venom

et al. 2013

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Summary Allergies are widely considered to be misdirected type 2 immune responses, in which IgE antibodies are produced against any of a broad range of seemingly harmless antigens. However, components of insect venoms also can sensitize individuals to develop severe IgE-associated allergic reactions, including fatal anaphylaxis, upon subsequent venom exposure. We found that mice injected with amounts of honeybee venom similar to that which could be delivered in one or two stings developed a specific type 2 immune response which increased their resistance to subsequent challenge with potentially lethal amounts of the venom. Our data indicate that IgE antibodies and the high affinity IgE receptor, FcεRI, were essential for such acquired resistance to honeybee venom. The evidence that IgE-dependent immune responses against venom can enhance survival in mice supports the hypothesis that IgE, which also contributes to allergic disorders, has an important function in protection of the host against noxious substances.

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Section: Introductionmentioning

confidence: 99%

A Beneficial Role for Immunoglobulin E in Host Defense against Honeybee Venom

et al. 2013

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“…There are several professions imposing a higher risk of exposure: pastry cookers, forestry workers and beekeepers. Among the latter group, the frequency of allergic reactions to bee stinging varies between 14 and 43% [5, 6]. In Poland, anaphylactic reactions most commonly develop after stings of the honeybee ( Apis mellifera, family Apidae) or the wasp ( Vespula vulgaris and Vespula germanica, family Vespidae, subfamily Vespinae).…”

Section: Introductionmentioning

confidence: 99%

Analysis of Safety, Risk Factors and Pretreatment Methods during Rush Hymenoptera Venom Immunotherapy

Górska

Chełmińska

Krzemieniecki

et al. 2008

Int Arch Allergy Immunol

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Background: The safety profile of venom immunotherapy is a relevant issue. We evaluated the frequency of severe adverse events (SAE), associated risk factors, retrospective comparison of pretreatment protocols including solely H₁ receptor blockers and a combination of H₁ and H₂ receptor blockers during rush Hymenoptera venom immunotherapy. Methods: The study group comprised 118 patients. The treatment was initiated according to a 5-day rush protocol with the use of standardized venom allergens of either wasp or honeybee. Results: During the rush induction, side effects occurred in 18 patients (15.2%), whereas SAE were present in 7 patients (5.9%). Twelve out of 18 (66.6%) developed anaphylactic reactions on the fourth day of the rush protocol, with the majority of cases at a dose of 40 or 60 µg of the venom extract (p = 0.001). The frequency of SAE was also significantly higher on the fourth day than thereafter (p = 0.0001) as well as in patients allergic to bee venom (p = 0.049). All systemic side effects were more frequent in women (p = 0.0065). However, this relation was not true when SAE were consider (p = 0.11). A higher percentage of SAE was observed in the subjects pretreated with both H₁ and H₂ receptor antagonists than in those pretreated with H₁ blocker only (8.8 vs. 4.1%); however, the difference was not significant. Conclusions: Considerable severity of allergic adverse events requires particular attention to patients allergic to bee venom and during rush phase, especially when rapidly increasing doses are administered. Pretreatment with H₂ blockers is debatable and warrants further investigation.

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“…Les souris développent une réponse T H 2 et la production d'IgE spécifiques du venin (Figure 2A) [9]. Chez l'homme, il est bien connu qu'une personne ayant déve-loppé des IgE en réponse à une piqûre d'abeille peut développer une réaction allergique, voire un choc anaphylactique fatal en cas de réexposition [6]. De manière surprenante, lorsque les souris ayant développé des IgE sont à nouveau exposées au venin, elles résistent mieux que les souris contrôles (Figure 2A Le développement d'une réponse immunitaire allergique peut avoir un effet bénéfique à l'encontre de venins En 1991 déjà, Margie Profet a émis l'idée controversée selon laquelle les réponses allergiques se sont maintenues en tant que mécanismes majeurs de défense de l'hôte à l'encontre de toxines [5].…”

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“…Cette hypothèse, non démontrée jusqu'à maintenant, est particulière-ment intéressante à nos yeux dans le contexte d'une catégorie d'allergènes, les venins. D'une part, les venins sont des substances toxiques responsables d'allergies chez l'homme [6]. D'autre part, nous avons montré précédemment …”

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