Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “WASPS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed2001

CR16 forms a complex with N-WASP in brain and is a novel member of a conserved proline-rich actin-binding protein family.

The Neuronal Wiskott-Aldrich syndrome protein (N-WASP) has emerged as a central regulator of the actin cytoskeleton with abilities to integrate multiple upstream signal inputs and transmit them to the Arp2/3 complex. Here, we demonstrate that native N-WASP is present in a tight complex with a proline-rich protein, CR16, which shares approximately 25% identity with WASP interacting protein. CR16 is encoded by a gene previously cloned as a glucocorticoid-regulated mRNA from a rat hippocampal cDNA library. Although N-WASP is expressed ubiquitously, full-length CR16 protein is found predominately in the brain. CR16 and N-WASP colocalize in primary hippocampal neurons and at the tips of their growth cone filopodia. In vitro, CR16 directly binds both monomeric and filamentous actin but does not affect the kinetics of actin polymerization mediated by N-WASP and the Arp2/3 complex. Sequence homologues of CR16 are found not only in other vertebrates but also in the invertebrate Caenorhabditis elegans and in yeast. Thus, CR16 and WASP interacting protein belong to a family of N-WASP-binding proteins.

Amino Acid Sequence↗
PubMed2001

Nck and phosphatidylinositol 4,5-bisphosphate synergistically activate actin polymerization through the N-WASP-Arp2/3 pathway.

The Wiskott-Aldrich syndrome protein (WASP) and its relative neural WASP (N-WASP) regulate the nucleation of actin filaments through their interaction with the Arp2/3 complex and are regulated in turn by binding to GTP-bound Cdc42 and phosphatidylinositol 4,5-bisphosphate. The Nck Src homology (SH) 2/3 adaptor binds via its SH3 domains to a proline-rich region on WASP and N-WASP and has been implicated in recruitment of these proteins to sites of tyrosine phosphorylation. We show here that Nck SH3 domains dramatically stimulate the rate of nucleation of actin filaments by purified N-WASP in the presence of Arp2/3 in vitro. All three Nck SH3 domains are required for maximal activation. Nck-stimulated actin nucleation by N-WASP.Arp2/3 complexes is further stimulated by phosphatidylinositol 4,5-bisphosphate, but not by GTP-Cdc42, suggesting that Nck and Cdc42 activate N-WASP by redundant mechanisms. These results suggest the existence of an Nck-dependent, Cdc42-independent mechanism to induce actin polymerization at tyrosine-phosphorylated Nck binding sites.

Actin-Related Protein 2↗
PubMed2002

Phosphorylation of tyrosine 291 enhances the ability of WASp to stimulate actin polymerization and filopodium formation. Wiskott-Aldrich Syndrome protein.

Wiskott-Aldrich Syndrome protein (WASp) is a key regulator of the Arp2/3 complex and the actin cytoskeleton in hematopoietic cells. WASp is capable of forming an auto-inhibited conformation, which can be disrupted by binding of Cdc42 and phosphatidylinositol 4,5-bisphosphate, leading to its activation. Stimulation of the collagen receptor on platelets and crosslinking the B-cell receptor induce tyrosine phosphorylation of WASp. Here we show that the Src family kinase Hck induces phosphorylation of WASp-Tyr(291) independently of Cdc42 and that this causes a shift in the mobility of WASp upon SDS-PAGE. A phospho-mimicking mutant, WASp-Y291E, exhibited an enhanced ability to stimulate actin polymerization in a cell-free system and when microinjected into primary macrophages induced extensive filopodium formation with greater efficiency than wild-type WASp or a Y291F mutant. We propose that phosphorylation of Tyr(291) directly regulates WASp function.

Actins↗
PubMed2006

Hyaluronan-CD44 interaction with neural Wiskott-Aldrich syndrome protein (N-WASP) promotes actin polymerization and ErbB2 activation leading to beta-catenin nuclear translocation, transcriptional up-regulation, and cell migration in ovarian tumor cells.

In this study we have investigated the interaction of hyaluronan (HA) and CD44 with the neuronal Wiskott-Aldrich syndrome protein (N-WASP) in regulating actin polymerization and ErbB2/beta-catenin signaling in human ovarian tumor cells (SK-OV-3.ipl cells). Biochemical and immunological analyses indicate that N-WASP is expressed in SK-OV-3.ipl cells and that the binding of HA stimulates N-WASP association with CD44 and Arp2/Arp3 leading to filamentous actin formation and ovarian tumor cell migration. In addition, HA binding promotes CD44-N-WASP association with ErbB2 and activates ErbB2 kinase activity that in turn increases phosphorylation of the cytoskeletal protein, beta-catenin. Subsequently, phosphorylated beta-catenin is transported into the nucleus leading to beta-catenin-mediated TCF/LEF-transcriptional co-activation. Because HA-induced beta-catenin phosphorylation, nuclear translocation, and TCF/LEF transcriptional activation is effectively blocked by the ErbB2 inhibitor, AG825, we conclude that HA/CD44-N-WASP-associated ErbB2 activation is required for beta-catenin-mediated signaling events. Transfection of SK-OV-3.ipl cells with N-WASP-VCA (verpolin homology, cofilin homology, and acidic domain) fragment cDNA not only blocks HA/CD44-induced N-WASP-Arp2/3 complex formation but also inhibits actin polymerization/F-actin assembly and tumor cell migration. Overexpression of the N-WASP-VCA domain also significantly reduces HA-induced ErbB2 recruitment to CD44, diminishes beta-catenin phosphorylation/nuclear translocation, and abrogates TCF/LEF-specific transcriptional co-activation by beta-catenin. Taken together, our findings strongly suggest that N-WASP plays a pivotal role in regulating HA-mediated CD44-ErbB2 interaction, beta-catenin signaling, and actin cytoskeleton functions that are required for tumor-specific behaviors and ovarian cancer progression.

Actins↗
PubMed1995

Identification of WASP mutations in patients with Wiskott-Aldrich syndrome and isolated thrombocytopenia reveals allelic heterogeneity at the WAS locus.

Mutation in the gene encoding the recently isolated WASP protein has now been identified as the genetic defect responsible for the X-linked Wiskott-Aldrich syndrome (WAS), a primary immunodeficiency disease associated with extensive phenotypic variability. To elucidate the range of WASP mutations responsible for WAS, we used PCR-SSCP analysis to screen for WASP gene mutation in 19 unrelated boys with the diagnosis of classical or attenuated WAS or isolated thrombocytopenia. All 19 patients had WASP mutations, each of which localized to the initial three or terminal three exons of the gene, and the majority of which were unique in each case. However, a missense mutation which results in substitution of the arginine at WAS codon 86 was identified in three boys with severe WAS as well as in one boy presenting with thrombocytopenia alone. While the three mutations found in the isolated thrombocytopenia patients leave the reading frame intact, about one-half of the gene alterations detected in both severe and attenuated WAS patients result in frameshifted transcript and premature translation termination. These findings therefore confirm the association of WAS with WASP mutation and identify WASP mutation as a cause for isolated congenital thrombocytopenia in males. While the WASP gene defects responsible for isolated thrombocytopenia and other mild presentations of WAS do not appear distinct from those resulting in severe WAS, these data indicate that analysis of WASP gene mutation provides a valuable tool for distinguishing the spectrum of WAS patients and the subset of males with isolated thrombocytopenia who represent mild cases of WAS.

Adolescent↗
PubMed2003

Regulation of actin dynamics by WASP family proteins.

Rapid reorganization of the actin cytoskeleton underlies morphological changes and motility of cells. WASP family proteins have received a great deal of attention as the signal-regulated molecular switches that initiate actin polymerization. The first member, WASP, was identified as the product of a gene of which dysfunction causes the human hereditary disease Wiskott-Aldrich syndrome. There are now five members in this protein family, namely WASP, N-WASP, WAVE/Scar1, 2, and 3. WASP and N-WASP have functional and physical associations with Cdc42, a Rho family small GTPase involved in filopodium formation. In contrast, there is evidence that links the WAVE/Scar proteins with another Rho family protein, Rac, which is a regulator of membrane ruffling. All WASP family members have a VCA domain at the C-terminus through which Arp2/3 complex is activated to nucleate actin polymerization. Analyses of model organisms have just begun to reveal unexpected functions of WASP family proteins in multicellular organisms.

Actins↗
PubMed2006

N-WASP inhibitor wiskostatin nonselectively perturbs membrane transport by decreasing cellular ATP levels.

Wiskott-Aldrich syndrome protein (WASP) and WAVE stimulate actin-related protein (Arp)2/3-mediated actin polymerization, leading to diverse downstream effects, including the formation and remodeling of cell surface protrusions, modulation of cell migration, and intracytoplasmic propulsion of organelles and pathogens. Selective inhibitors of individual Arp2/3 activators would enable more exact dissection of WASP- and WAVE-dependent cellular pathways and are potential therapeutic targets for viral pathogenesis. Wiskostatin is a recently described chemical inhibitor that selectively inhibits neuronal WASP (N-WASP)-mediated actin polymerization in vitro. A growing number of recent studies have utilized this drug in vivo to uncover novel cellular functions for N-WASP; however, the selectivity of wiskostatin in intact cells has not been carefully explored. In our studies with this drug, we observed rapid and dose-dependent inhibition of N-WASP-dependent membrane trafficking steps. Additionally, however, we found that addition of wiskostatin inhibited numerous other cellular functions that are not believed to be N-WASP dependent. Further studies revealed that wiskostatin treatment caused a rapid, profound, and irreversible decrease in cellular ATP levels, consistent with its global effects on cell function. Our data caution against the use of this drug as a selective perturbant of N-WASP-dependent actin dynamics in vivo.

Actin-Related Protein 2-3 Complex↗
PubMed2004

WASp deficiency in mice results in failure to form osteoclast sealing zones and defects in bone resorption.

No defects related to deficiency of the Wiskott-Aldrich Syndrome protein (WASp) have been described in osteoclasts. Here we show that there are significant morphologic and functional abnormalities. WASp-null cells spread over a much larger surface area and are highly polykaryotic. In their migratory phase, normal cells assemble clusters of podosomes behind their leading edges, whereas during the bone resorptive phase multiple podosomes are densely aggregated in well-defined actin rings forming the sealing zone. In comparison, WASp-null osteoclasts in either phase are markedly depleted of podosomes. On bone surfaces, this results in a failure to form actin rings at sealing zones. Complementation of WASp-null osteoclasts with an enhanced green fluorescent protein (eGFP)-WASp fusion protein restores normal cytoarchitecture. These structural disturbances translate into abnormal patterns of bone resorption both in vitro on bone slices and in vivo. Although physiologic steady-state levels of bone resorption are maintained, a major impairment is observed when WASp-null animals are exposed to a resorptive challenge. Our results provide clear evidence that WASp is a critical component of podosomes in osteoclasts and indicate a nonredundant role for WASp in the dynamic organization of these actin structures during bone resorption.

Actin Cytoskeleton↗
PubMed2000

Mutations of the WASP gene in 10 Japanese patients with Wiskott-Aldrich syndrome and X-linked thrombocytopenia.

Wiskott-Aldrich syndrome (WAS) is an X-linked recessive disorder characterized by thrombocytopenia, immunodeficiency, and eczema. X-linked thrombocytopenia (XLT) is a mild form of WAS with isolated thrombocytopenia. Both phenotypes are caused by mutation of the Wiskott-Aldrich syndrome protein (WASP) gene. In this study, we identified mutations of the WASP gene in 10 Japanese patients from 9 unrelated families with WAS/XLT. All XLT patients (n = 3) and one WAS patient had a missense mutation at the PH domain of WASP. Two WAS patients had nonsense mutations. One WAS patient had exon 8 skipping caused by one nucleotide deletion at the acceptor site of intron 7. Three WAS patients had genomic deletions; one of the three had a large genomic deletion involving exons 3 to 7. Codons 45 and 86 seem to be the hot spots of the WASP mutation, because missense mutations in these codons have been reported previously in several WAS/XLT patients in addition to the patients in this report, and patients with the same mutation show a similar clinical phenotype. All other mutations are novel, indicating that the mutations of WASP are heterogeneous. EB virus-transformed cell lines from XLT patients expressed nearly normal amounts of WASP, whereas those from typical WAS patients expressed almost undetectable amounts of WASP. We conclude that the analysis of gene mutation and protein expression of WASP are useful together in assessing the severity of WAS.

Adult↗
PubMed2003

[Identification of two novel WASP gene mutations in 3 boys with Wiskott-Aldrich syndrome].

OBJECTIVE: The Wiskott-Aldrich syndrome (WAS) is a rare X-linked primary immunodeficiency caused by mutations in the WAS protein (WASP) gene. The disease is characterized by recurrent infections, eczema, and thrombocytopenia with small platelets, and it is known to be associated with extensive clinical variability, and mutation studies indicated that genotypes are also highly variant among WAS patients. The present study was conducted to identify the mutation types of Wiskott-Aldrich syndrome protein (WASP) gene in 3 boys suffering from Wiskott-Aldrich syndrome. METHODS: Based on the typical clinical manifestations of Wiskott-Aldrich syndrome including thrombocytopenia, eczema, and recurrent infections and scanning electron micrographs, 3 patients were suspected of having WAS. The WASP gene of the 3 patients and their mothers were detected by PCR-direct sequencing analysis. RESULTS: By sequence analysis using sense and antisense primer separately, the authors found two novel WASP gene mutations. For the twin brothers, a C deletion at nucleotide 984 was detected in exon 10 of WASP gene (984delC). The consequence of the C deletion involved frameshift mutation after H317 and premature stop at 444 (H317fsX444). Their mother was a carrier of the mutated WASP gene. For another WAS patient, a nonsense mutation with nucleotide substitution of G to T at position 1388 (1388G-->T) in exon 11 of WASP gene, led to premature translational termination at amino acid position 452 (E452X). His mother had not been found to have WASP gene mutation. CONCLUSION: Genetic analysis is useful in definite diagnosis of Wiskott-Aldrich syndrome patients and in carrier detection and prenatal diagnosis, especially of atypical or sporadic WAS patients.

Blood Platelets↗
PubMed1996

N-WASP, a novel actin-depolymerizing protein, regulates the cortical cytoskeletal rearrangement in a PIP2-dependent manner downstream of tyrosine kinases.

Here we identify a 65 kDa protein (N-WASP) from brain that binds the SH3 domains of Ash/Grb2. The sequence is homologous to Wiskott-Aldrich syndrome protein (WASP). N-WASP has several functional motifs, such as a pleckstrin homology (PH) domain and cofilin-homologous region, through which N-WASP depolymerizes actin filaments. When overexpressed in COS 7 cells, the wild-type N-WASP causes several surface protrusions where N-WASP co-localizes with actin filaments. Epidermal growth factor (EGF) treatment induces the complex formation of EGF receptors and N-WASP, and produces microspikes. On the other hand, two mutants, C38W (a point mutation in the PH domain) and deltaVCA (deletion of the actin binding domain), localize predominantly in the nucleus and do not cause a change in the cytoskeleton, irrespective of EGF treatment. Interestingly, the C38W PH domain binds less effectively to phosphatidylinositol 4,5-bisphosphate (PIP2) than the wild-type PH domain. These results suggest the importance of the PIP2 binding ability of the PH domain and the actin binding for retention in membranes. Collectively, we conclude that N-WASP transmits signals from tyrosine kinases to cause a polarized rearrangement of cortical actin filaments dependent on PIP2.

Actins↗
PubMed2006

Age and diet influence the composition of venom from the endoparasitic wasp Pimpla turionellae L. (Hymenoptera: Ichneumonidae).

Venom from the endoparasitic wasp Pimpla turionellae L. (Hymenoptera: Ichneumonidae) was found to contain a complex mixture of biogenic amines, noradrenalin, phospholipase B, and several proteins and peptides. The amount of noradrenalin and serotonin was found to be highest in venom from newly emerged wasps and decreased with age. Histamine was detected in minute amounts in comparison to the other venom components, and declined with increasing age of the parasitoids. Total peptides and proteins detected by reversed-phase HPLC increased with host age. Old-aged (30-33 days after emergence) wasps contained 2-fold more phospholipase B than young (<10 days [d] old) or medium-aged (10-22-d-old) females. Increases in phospholipase B alone, however, did not account for all changes in total venom protein because by 40 days after emergence, the levels of this enzyme began to decline while the amount of total protein was higher than in younger wasps. For all venom components detected, the amount present in the venom sharply decreased following host exposure. This was presumed to be the result of venom depletion associated with envenomation. Consistent with this view were the modest increases in venom components in wasps displaying a decreased rate of parasitization. When adult females were offered honey alone or in combination with feeding on hosts, no significant changes in venom composition were observed, with the exception of noradrenalin, which was found to be 5 times higher in concentration in wasps fed honey only. These results suggest that wasp age and incidence of parasitism are more important features influencing the composition of venom than the diet of adult females.

Age Factors↗
PubMed2006

[Increasing incidence of wasp stings in otorhinolaryngological practice].

BACKGROUND: Wasp sting injuries can be lethal due to generalized reactions and edematous obstruction of the upper respiratory system. Due to media reports and our own observations, the consequences of the 2004 "plague of wasps" should be examined for the ear, nose, and throat (ENT) region. PATIENTS AND METHODS: Wasp sting injuries treated during the years 2002 to 2004 were evaluated in a retrospective study with respect to frequency, localization, therapy, occurrence of allergic reactions, and other complications. RESULTS: In 2002 to 2004, the number of patients with wasp sting injuries tripled. The occurrence of stings in the ENT region increased from 20% to more than 40%, with a strong rise in enoral and endolaryngeal stings after accidental swallowing or inhalation of wasps. The medical treatments employed proved the existence of sufficient therapeutic strategies. CONCLUSIONS: The treatments demonstrate a clear increase in wasp sting injuries in the year 2004. The main climatic cause was the European record summer of 2003, in which wasps multiplied.

Adolescent↗
PubMed2005

Nest paper absorbency, toughness, and protein concentration of a native vs. an invasive social wasp.

The amount of proteinaceous food that was allocated to nest construction by a native wasp (Polistes fuscatus) vs. an invasive wasp (Polistes dominulus) in North America was examined following a field experiment under natural and surplus prey foraging conditions. Wasps of the surplus prey foraging conditions were provided with prey ad libitum within an enclosed area, while wasps of the natural treatment foraged in an adjacent field-woodland site. At the end of the field experiment, each nest was tested for water absorbency, toughness, and protein concentration. The hypotheses were: (1) When all nests are equally sheltered, the invasive P. dominulus (PD) allocates less protein to nest paper construction (for waterproofing and strengthening) and more protein to developing larvae than the native P. fuscatus (PF). (2) Nests of P. dominulus are more absorbent (less waterproof) and less tough than nests of P. fuscatus. Results indicate that P. fuscatus nests from surplus prey foraging conditions were more absorbent (less waterproof) to artificial rain drops than P. dominulus nests. The toughness of nests was similar between wasp species. However, nests from the natural treatment were tougher than those from the surplus prey treatment. Nests from the natural foraging conditions had half as much protein as those from surplus prey foraging conditions. There was no correlation between nest protein concentration and the number of prey taken, the number of cells, the number of adult offspring produced, or the total wasp biomass produced per colony. For PF under surplus prey conditions, protein concentration and absorbency were negatively correlated, but for PD the correlation was positive. In conclusion, when prey were scarce, Polistes wasps allocated less protein to nest construction. Also, the introduced P. dominulus may increase production of offspring by allocating less to nest construction than that of the native P. fuscatus, and so more protein to offspring production.

Adaptation, Physiological↗
PubMed2003

Storage proteins in vespid wasps: characterization, developmental pattern, and occurrence in adults.

Wasps of family Vespidae contain three types of major proteins that have the size, amino acid composition, subunit composition, immunological reactivity, and pattern of occurrence characteristic of storage proteins. The three types of storage protein, which have been identified in other Hymenoptera, are very high density lipoprotein, high glutamine/glutamic acid protein, and hexamerin. The predominant pattern of occurrence for these proteins is as known from most or all Holometabola: synthesis during the last larval instar and utilization as an amino acid source during metamorphosis. Hexamerin also occurred in a large young adult female Monobia quadridens but not a small one, which suggests that carry-over into adult females is a reaction norm response to quantity of larval provisions, because these wasps could not have fed as adults. In two paper wasp species of the genus Polistes, hexamerin was present in large adult females which emerged during the colony cycle phase when reproductive females are typically produced, but not in adult female offspring that emerged earlier in the colony cycle or in adult females that were workers. It cannot be confirmed by these data that the hexamerin in the adult paper wasps represented carry-over from metamorphosis rather than post-emergence feeding, but the pattern of occurrence suggests that presence of storage protein may play a role in caste differentiation in paper wasps. No storage protein was found in any adult Vespula maculifrons, a yellowjacket wasp, suggesting that caste differentiation in vespine wasps does not incorporate storage protein as a component.

Amino Acids↗
PubMed2001

Volatiles from Ficus hispida and their attractiveness to fig wasps.

Volatile compositions of receptive (ready to be pollinated), postpollinated, and postparasitized figs. and leaves of Ficus hispida were analyzed. Differences among them were examined, and the specificity of fig wasp attractiveness was investigated. Linalool was the major constituent of steam-distilled oil of either male or female receptive figs, while dibutyl phthalate was the major compound of the oils of postparasitized and postpollinated figs. In petroleum ether extracts, palmitic oil, and 9,12-octadecadienoic acid were the main constituents of male and female receptive figs, while hexadecanoic acid ethyl ester was the major compound of postparasitized and postpollinated figs. In dichloromethane extracts, linalool was the major constituent of male and female receptive figs, 1-hydroxylinalool was the major component of male postparasitized figs, and 1-hydroxylinalool and benzyl alcohol were the major constituents of female postpollinated figs. Bioassays with sticky traps showed that Ceratosolen solmsimarchal was attracted to dichloromethane extracts of male and female receptive figs and to petroleum ether extracts of female receptive figs, but was not attracted to dichloromethane and petroleum ether extracts of male postparasitized and female postpollinated figs. Figs were attractive to pollinating wasps only at the receptive stage. The volatile constituents of receptive figs were different from those of postpollinated or postparasitized figs. From a receptive to a postpollinated state, figs changed in their volatile composition. Some compounds disappeared or decreased in amount. These include linalool, linalool oxide, alpha-terpeneol, and 2,6-dimethyl-1,7-octadiene-3,6-diol, which may act as the attractants of the wasps. Others increased in amount, or several additional chemicals appeared. These include dibutyl phthalate, 1-hydroxylinalool, and benzyl alcohol, which may be repellents of the wasps. That dichloromethane extracts of male and female receptive figs showed similar activities in attracting fig wasps indicates that receptive figs of both sexes are similarly attractive to fig wasps, which is further supported by their similar volatile composition. Leaf extract was not attractive to the wasps.

Animals↗
PubMed2004

Oviposition strategies, host coercion and the stable exploitation of figs by wasps.

A classic example of a mutualism is the one between fig plants (Ficus) and their specialized and obligate pollinating wasps. The wasps deposit eggs in fig ovules, which the larvae then consume. Because the wasps derive their fitness only from consumed seeds, this mutualism can persist only if the wasps are prevented from laying eggs in all ovules. The search for mechanisms that can limit oviposition and stabilize the wasp-seed conflict has spanned more than three decades. We use a simple foraging model, parameterized with data from two Ficus species, to show how fig morphology reduces oviposition rates and helps to resolve the wasp-seed conflict. We also propose additional mechanisms, based on known aspects of fig biology, which can prevent even large numbers of wasps from ovipositing in all ovules. It has been suggested that in mutualistic symbioses, the partner that controls the physical resources, in this case Ficus, ultimately controls the rate at which hosts are converted to visitors, regardless of relative evolutionary rates. Our approach provides a mechanistic implementation of this idea, with potential applications to other mutualisms and to theories of virulence.

Animals↗
PubMed1995

The incidence and nature of adverse reactions to injection immunotherapy in bee and wasp venom allergy.

The incidence, time course and nature of systemic reactions to injections of bee and wasp venom during immunotherapy have been estimated in an open, prospective, single centre study. One hundred and nine survivors of moderate to severe systemic reactions to stings from hymenoptera, received courses of bee or wasp venom by monthly subcutaneous injection for up to 3 years. Systemic reactions were recorded after 7.5% of 946 weekly venom injections during the initial phase of treatment, and after 2.1% of 1789 monthly maintenance injections. In both phases of treatment, reactions were more frequent after bee (17% of initial phase, 7.8% of maintenance treatment) than after wasp (3% of initial phase, 0.3% of maintenance treatment) venom injections. The percentage of patients experiencing at least one reaction was also higher for bee (46%) than for wasp (14%) sensitive patients. Over 80% of reactions began within 30 min of injection, over 90% within 1 h and only two (2%), between 1 and 2 h, the remaining six (5.5%) starting more than 2 h after injection. Only 0.47% of venom injections produced a systemic reaction which was severe enough to require adrenaline treatment. The female patients experienced more reactions (21% of the wasp, 60% of the bee, sensitive) than the males (5.5% wasp, 20% bee). Age and atopy did not appear to be significant risk factors for systemic reactions. We conclude that wasp and bee venom immunotherapy in a conventional dosage regimen was generally well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗