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After 70% of the rat liver volume has been resected, certain stimulating effect of a single administration of bee venom (1 mg/kg) on hepatocyte proliferation is revealed. In 4 hours the amount of binuclear hepatocytes increases, and in 22-24 hours increases their mitotic activity. The effect of bee venom is explained as activation of the adenilate cyclase system by means of prostaglandins and adrenal hormones.
The bee and cobra venom phospholipases A2 as well as partially acetylated cobra venom phospholipase A2 are studied for their effect on phospholipid composition of synaptosomes and their Mg2+- and Na+,K+-ATPase activity. It is established that these phospholipases induce the splitting of phosphatidylethanolamine, phosphatidylcholine and phosphatidylserine, inhibition of the Na+,K+-ATPase activity and activation of Mg2+-ATPase. Bee venom phospholipase A2 is more effective than cobra venom phospholipase A2, the both phospholipases splitting phosphatidylethanolamine most intensively. The ATPase activity may be partially or completely restored by exogenic phosphatidylcholine and phosphatidylserine; exogenic phosphatidylethanolamine is not efficient in this respect.
Pesticide residues are usually determined by physical, chemical and biological methods. The simplicity and adaptability of bioassay methods have won their acceptance in the field of residue analysis. Theoretically, any organism that is susceptible to a pesticide may be used for its bioassay in any environmental sample. This means that such organism may serve as a bioindicator for the detection of certain pollutants. The susceptibility of honey bees (Apis melifera L.) to many insecticides commonly used in crop protection led to an attempt to use it as a bioindicator for the determination of residues of some insecticides in plant materials, as well as to detect toxicity hazards to honey bees of some commonly used insecticides. Results of this work which have been recently published may suggest "Yes" to answer the question posed in the title of this subject.
We have measured in allergic and non-allergic beekeepers IgE and IgG antibodies to the bee venom allergens, phospholipase A2 (PLA2) and hyaluronidase (HYAL), by the radioallergosorbent test (RAST) and a 125I-radiolabelled antigen-binding assay. The absolute amount of IgG antibody in a reference serum was determined by saturation analysis using 125I-radiolabelled PLA2 and HYAL. Using monoclonal anti-IgE coated microtitre plates, the absolute amount of IgE antibody to the same antigen was also determined by saturation analysis. Regardless of the IgE response to the different allergens, IgG antibody concentrations to PLA2 were invariably higher than those to HYAL. In addition, the ratio of IgG to IgE antibody was higher for PLA2 (220:1) than for HYAL (10:1). Higher levels of IgG antibody to both allergens (especially HYAL) were found in those who had had prolonged exposure to bee stings. These data suggest that the level of IgG antibody produced is related to the dose administered, while the amount of IgE antibody may be regulated by other factors.
Bee venom allergy is a common problem in South Africa, and although most patients develop only local reactions after a sting, generalized life-threatening reactions may occur. Immunotherapy with purified bee venom has proved effective in preventing subsequent sting anaphylaxis. However, because of side-effects during a course of desensitization, the high cost of this form of therapy and the extended period for which therapy may be required, careful patient selection is essential. Only patients with documented generalized reactions should be considered for therapy. Patients with severe local reactions, and those with urticaria or other cutaneous symptoms, should not undergo desensitization. Although it is not yet known for how long desensitization should continue, a negative skin test 3-6 years after the initiation of therapy suggests that desensitization can be discontinued.
The authors injected 3 groups of pregnant rats with 1/5 of LD50 of whole bee venom and its low and high weight molecular fractions daily between the 6th and 14th day of gestation. The embryos of the treated animals, aged 20 days, showed a reduction of the weight and dimunution of the activity of lactate dehydrogenase and isocitrate dehydrogenase in their liver homogenate. There were autolisis and dead rats in the uterus of the treated animals (embryotoxic effect). There were no teratogenic alterations. The low weight molecular fraction of the bee venom revealed more manifested embryotoxic effect.
The allergy to bee venom is dangerous and life threatening. Skin tests and immunotherapy should be done with bee venom extracts. The RAST proves to be helpful if blood taking is done within a short period after stinging. In the meantime immunotherapy should be given lifelong and total and specific IgE antibodies controlled. In addition we believe that the determination of IgG-blocking antibodies is important.
The author reports on a 39 year-old male patient with allergic asthma who died several hours after a bee sting in a state of shock. While IgE antibodies were not present, distinct deposits of IgG4 antibodies in the kidney and lung were demonstrated for the first time after a bee sting. The intention of this report is to stress the importance of hyposensibilisation of patients with an allergic condition after determination of the relevant class or subclass of immunoglobulins.
Lewis rats were immunized with bee venom allergen in Freund's complete adjuvant (FCA) or with FCA only. Animals immunized with bee venom developed specific IgG antibodies but no specific IgE antibodies were detected. Lymphocytes from lymph nodes when cultured with antigen in vitro showed an increased stimulation index from day 17 onwards. A concomitant augmentation of T suppressor cells was observed; the T helper/T suppressor cell ratio declined from 4.5:1 before immunization to 1:1 from day 5 onwards.
The effect of presynaptic neurotoxin from bee and cobra venom--phospholipases A2 on Na+-dependent high affinity [14C]choline transport from the striate body of rat brain into synaptosomes has been studied. It was shown that both phospholipases A2 inhibit the re-uptake of [14C]choline and specifically stimulate the release of [14C]acetylcholine from the synaptosomes. This effect is especially well-pronounced for bee venom phospholipase A2. It was assumed that damages of biochemical processes on the presynaptic membrane result in a blockade of synaptic transmission in nerve-muscle preparations.
Human basophil degranulation responses to grass pollen and whole bee venom as allergens and to anti-IgE and anti-IgG4 as antibodies in hay fever and bee venom allergic patients were assessed using a flow-cytometric system. The concordance of basophil degranulation with skin tests and RAST assays reached more than 90%. These allergens and antibodies could degranulate basophils in a dose-dependent manner; however, there was a wide variation in the response of basophils obtained from different individuals. Moreover, a significant correlation was observed between the degree of degranulation by allergens and anti-IgE, or by allergens and anti-IgG4, but this was not the case between serum IgE concentrations and basophil response to anti-IgE. These data suggest that 'releasability' of basophils upon challenge by allergens and antibodies is also an important parameter in determining the degree of hypersensitivity in each subject.
Mastcell-degranulating peptide from bee venom exhibits anti-inflammatory activity in the Carrageenine-inflammation model on mice and rats. Its dose/response relationship corresponds to that of dexamethasone. In the 125I-rat serum albumin-test the substance shows an inhibitory effect of 87% on the developing Carrageenine edema at a dose of 1 mg/kg; in contrast the bee venom peptides apamin and melittin exhibit small edema supressing effects. The anti-inflammatory characteristics of MCD-peptide have to be considered with regard to its high basicity and specific molecular structure, determined by two disulfide-bridges for the derivaties with acetylated amino groups respectively with alkylated cysteine residues show no significant activity. A pentapeptide in the C-terminal region of MCD-peptide (Lys-Ile-Cys-Gly-Lys)2 inhibits the carrageenin edema to 55% at a dose of 10 mg/kg.
The molecular and cellular mechanisms controlling Ab isotype selection following encounter of a given Ag are still unclear, although the regulatory role of cytokines is established. In the present study we explored the possibility that the nonimmunologic interaction of an allergen with cells of the innate immune system might result in a release of mediators that promote IgE isotype selection in adaptive responses. Using the bee venom allergen phospholipase A2 (PLA2) and a mutant variant lacking enzymatic function, we show that PLA2, but not its catalytically inactive variant, is able to induce IgE-independent mediator release, including IL-4, from rodent mast cells. Assessing the in vivo relevance of these observations, we find that repeated injections of low doses of active enzyme into mice induce the synthesis of high levels of PLA2-specific IgE, while immunization with the inactive form yields no detectable IgE response. Both Ags were similarly immunogenic when high doses of Ag were used for immunization. These findings suggest that mast cells might be a source of IL-4 at the onset of specific immunity against sources of allergens such as bee venom that contain PLA2 and support the concept that the biologic action of an Ag on cells of the innate immune system can play a role in determining adaptive immune responses.
Clinical study was conducted on 77 adult patients with hypersensitivity to honey bee venom (HBV) to determine clinical characteristics and pathogenesis of hypersensitivity to HBV as well as the effect of specific immunotherapy(ITS) with HBV on several clinical and immunological parameters. The patients studied (43 women and 34 men of age ranging between 18-61 years with a mean age at 30 years) were divided into two groups: Group 1-44 patients with a history of anaphylactic shock following honey bee sting, who received specific immunotherapy with HBV. Group 2-33 patients hypersensitive to HBV(9 people reacted with severe anaphylactic systemic reaction, while others had skin reactions) who were not treated by ITS method. In all patients skin tests with HBV allergen were conducted before and at various stages of immunotherapy. Specific IgE (I1), s-IgG4 (I1), total IgE, IgG, IgA, IgM, C3c, C4 were estimated in sera samples obtained at the beginning, during the course and at the end of ITS. Dynamics of changes of these parameters were studied during a 3-year period of ITS. The challenge tests were conducted at the end of the treatment. 86.9% of treated patients reacted with IgE-mediated reactions. They showed elevated levels of s-IgE before immunotherapy, and significant decrease in s-IgE and increase in s-IgG4 titers after ITS. 10.4% of patients showed clinical symptoms of anaphylaxis, but non-IgE mediated. IgE titer in these patients was < or = 0.2 IU/ml and has not significantly changed during immunotherapy. s-IgG, levels were in these patients below 2 micrograms/ml.(ABSTRACT TRUNCATED AT 250 WORDS)
In the human immune response to the main bee venom allergen phospholipase A2 (PLA2), Abs of the IgG4 isotype are associated with protection. The antigenic sites of PLA2 that are recognized by two mAb of this isotype have been analyzed at the molecular level. The interaction of PLA2 with these two Abs has previously been shown to depend on the conformation of the Ag and to be sensitive to lysine modifications. Therefore, genetically engineered Ag displaying single point mutations of lysine residues were generated. Nine out of twelve surface-exposed lysine residues were substituted by glutamate or glutamine, and the effect of individual mutations on mAb binding was analyzed in the context of the folded Ag. Substitution of lysine at position 25 with either glutamate or glutamine completely abrogates binding to both mAb. All other mutants do not show a difference in binding when compared with wild-type Ag. Probing of sera from bee keepers with lysine 25 mutants reveals that a significant proportion of serum Abs of the IgG4 isotype display specificity for this epitope, suggesting that this represents a major B cell-antigenic site in hyperimmune individuals. We further found that both mAbs inhibit the catalytic activity of PLA2, a property that may account for the protective role of IgG4 Abs in hyperimmune individuals.
Even a single honeybee sting can lead to anaphylaxis in a susceptible person, but severe reactions can result from multiple stings, particularly if stings are from the fast-spreading Africanized honeybees, sometimes called "killer" bees. Signs and symptoms of multiple stings may include urticaria, nausea, vomiting, diarrhea, hypotension, confusion, seizures, and renal failure. Treatment is entirely supportive and requires special attention to airway patency, blood pressure, and renal function. Patients with more than 50 stings are at a higher risk of toxicity. Stingers should be removed by scraping gently to prevent further venom injection. Smoke or aerosolized deet (diethyl-toluamide) may thwart attacking bees, but avoidance is the best line of defense.
The authors report a case of limited inferior myocardial infarction in a young man following a bee sting. Coronary angiography, performed following the acute phase, showed angiographically healthy coronary arteries and minimal sequelae of myocardial necrosis in the inferior territory. The pathogenic role of the bee sting in myocardial necrosis was suggested by the timing of the events. The probable mechanism responsible for this myocardial infarction was severe coronary arterial spasm (partly mediated by psychological stress related to the intensity of the anaphylactic reaction) with secondary in situ thrombosis probably facilitated by cardiovascular collapse. The role of anaphylaxis, generating acute coronary insufficiency, is discussed in the light of this clinical case.
Lectin-like properties of bee venom proteins were studied. Phospholipase A2 was demonstrated to harbor lectin activity. Specific hemagglutinating activity of the isolated phospholipase exceeded 320 times the activity of the initial bee venom.