Cross-Reactivity between Oak and Birch Pollens in Korean Tree Pollinosis.

Oak and birch trees belong to Fagales order. Specific IgE to pollen allergens of both trees are frequently found in Korea pollinosis patients. Oak trees which comprise 40% of forest area are common in Korea. However, birch trees are sparse. We compared the allergenicity of pollen extracts of white oak, sawtooth and Mongolian oaks which are prevalent species in Korea, with the pollen extract of birch. The cross-reactivity of four pollen extracts was examined with pooled sera of 12 patients by ELISA, immunoblotting and CAP inhibitions. A protein of 17 kDa, putatively homologous to a major birch allergen Bet v 1, displayed strong IgE reactivity from white oak and sawtooth oak pollen extract but not from Mongolian oak pollen. Notably, a 23-kDa protein from sawtooth and white oaks showed strong IgE reactivity and inhibited by Bet v 1. IgE binding to white oak was inhibited a maximum of 94.6% by white oak, 93.4% by sawtooth oak, 83.2% by Mongolian oak, and 68.8% by birch. Furthermore, sawtooth oak, white oak, and Mongolian oak extracts were able to inhibit up to 78.5%, 76.6% and 67.3% of IgE binding to birch extract, while birch extract itself inhibited up to 94.3%. Specific IgE to Bet v 1 was inhibited a maximum of 79.1% by sawtooth oak, 77.4% by white oak, and 72.7% by Mongolian oak, while 81.5% inhibition was shown by birch. Bet v 1 was able to partially inhibit its homologous molecules from sawtooth oak and white oak in immunoblotting. Birch pollen extract was found to be cross-reactive primarily with Bet v 1-homologous allergen from oak pollens in Korea pollinosis patients. Considering the sparseness of birch tree in Korea, oak, especially sawtooth oak may be the main cause of tree pollinosis in Korea, rather than birch.

A novel human anti-VCAM-1 monoclonal antibody ameliorates airway inflammation and remodelling.

Asthma is a chronic inflammatory disease induced by Type 2 helper T cells and eosinophils. Vascular cell adhesion molecule-1 (VCAM-1) has been implicated in recruiting eosinophils and lymphocytes to pathological sites in asthma as a regulatory receptor. Accordingly, monoclonal antibody (mAb) against VCAM-1 may attenuate allergic inflammation and pathophysiological features of asthma. We attempted to evaluate whether a recently developed human anti-VCAM-1 mAb can inhibit the pathophysiological features of asthma in a murine asthma model induced by ovalbumin (OVA). Leucocyte adhesion inhibition assay was performed to evaluate the in vitro blocking activity of human anti-VCAM-1 mAb. OVA-sensitized BALB/c mice were treated with human anti-VCAM-1 mAb or isotype control Ab before intranasal OVA challenge. We evaluated airway hyperresponsiveness (AHR) and bronchoalveolar lavage fluid analysis, measured inflammatory cytokines and examined histopathological features. The human anti-VCAM-1 mAb bound to human and mouse VCAM-1 molecules and inhibited adhesion of human leucocytes in vitro. AHR and inflammatory cell counts in bronchoalveolar lavage fluid were reduced in mice treated with human anti-VCAM-1 mAb as compared with a control Ab. The levels of interleukin (IL)-5 and IL-13, as well as transforming growth factor-ß, in lung tissue were decreased in treated mice. Human anti-VCAM-1 mAb reduced goblet cell hyperplasia and peribronchial fibrosis. In vivo VCAM-1 expression decreased in the treated group. In conclusion, human anti-VCAM-1 mAb attenuated allergic inflammation and the pathophysiological features of asthma in OVA-induced murine asthma model. The results suggested that human anti-VCAM-1 mAb could potentially be used as an additional anti-asthma therapeutic medicine.

Spontaneously reported hepatic adverse drug events in Korea: multicenter study.

Hepatic adverse drug reactions (ADRs) to certain drugs may differ within each country, reflecting different patterns of prescription, socioeconomic status, and culture. The purpose of this study was to assess the suspected cause of hepatic ADRs using the spontaneously reported pharmacovigilance data from Korea. A total of 9,360 spontaneously reported adverse drug events (ADEs) from nine Pharmacovigilance Centers were analyzed. Risk of hepatic ADEs was assessed by calculating the reporting odds ratio (ROR). Of the 9,360 cases, 567 hepatic ADEs were reported. The most frequently prescribed drug classes inducing hepatic ADEs were anti-tuberculotics, cephalosporins, valproic acids, penicillins, quinolones, non-steroidal anti-inflammatory drugs (NSAIDs), anti-viral agents, and statins. ROR values were especially high in anti-tuberculosis drugs, systemic antifungal drugs for systemic use, anti-epileptics, propylthiouracil, and herbal medicines. Underlying diseases such as tuberculosis (6.9% vs 0.9%), pneumonia (4.9% vs 1.7%), intracranial injury including skull fracture (4.5% vs 0.9%), HIV (3.4% vs 0.4%), subarachnoid hemorrhage (2.8% vs 0.5%), and osteoporosis (2.4% vs 1.4%) were significantly more common in hepatic ADE group. In conclusion, anti-infective drugs, anti-epileptics, NSAIDs and statins are the most common suspects of the spontaneously reported hepatic ADEs, in Korea. Careful monitoring for such reactions is needed for the prescription of these drugs.

Sequence polymorphisms of Der f 1, Der p 1, Der f 2 and Der p 2 from Korean house dust mite isolates.

Amino acid sequence variations have possible influences on the allergenicity of allergens and may be important factors in allergen standardization. This study was undertaken to investigate the sequence polymorphisms of group 1 and 2 allergens from Korean isolates of the house dust mites Dermatophagoides farinae and D. pteronyssinus. cDNA sequences encoding group 1 and 2 allergens were amplified by RT-PCR and compared the deduced amino acid sequences. Der f 1.0101, which appeared in 64.0 % of the 50 sequences analyzed, was found to be predominant. Among the Der p 1 sequences, Der p 1.0102 and 1.0105 were predominant (58 %). Among the Der f 2 sequences, Der f 2.0102 (40.7 %) and a new variant with Gly at position 42 (27.8 %) were predominant. The deduced amino acid sequences of 60 Der p 2 clones were examined, and 28 variants with 1-5 amino acid substitutions were found. Interestingly, all of the Der p 2 sequences had Thr instead of Lys at position 49. Two variants (Leu40, Thr49, and Asn114 (26.6 %); Val40, Thr49, and Asn114 (20.0 %)) were found to be the most predominant forms of Der p 2. Der p 1 has a high rate of sporadic substitutions and the group 2 allergens show a more regular pattern with orderly associations of amino acid substitutions. Der f 1 and Der p 2 from Korean mite isolates have unique amino acid sequence polymorphisms. These findings provide important data for house dust mite allergen standardization.

A possible association of EMID2 polymorphisms with aspirin hypersensitivity in asthma.

Aspirin-intolerant asthma (AIA) is an asthma phenotype characterized by the development of bronchoconstriction following ingestion of aspirin. Despite the well-defined pathological trigger, the underlying mechanisms of AIA are still unclear. With the biophysical characteristics of the human EMI domain-containing protein 2 (EMID2) gene in relation to the extracellular matrix deposition and epithelial-mesenchymal transition as pivotal characteristics of airway remodeling in asthma, we hypothesized that genetic polymorphisms of EMID2 might affect the development of AIA. In this study, the allelic associations of 49 single-nucleotide polymorphisms (SNPs) of the human EMID2 gene were evaluated from 163 AIA patients and 429 aspirin-tolerant asthma (ATA) subjects as controls in a Korean population. Logistic analysis showed that five SNPs (P = 0.01-0.04, but P (corr) > 0.05) and EMID2_BL2_ht2 haplotype (unique to the minor alleles of rs4727494 and rs13233066; P = 0.02; P (corr) = 0.02) were significantly associated with AIA. More interestingly, regression analysis of the decline of forced expiratory volume in one second (FEV(1)) by aspirin provocation revealed that 10 SNPs (P = 0.003-0.04) and four relevant haplotypes (P = 0.002-0.02) were significantly associated with the fall rate of FEV(1) by aspirin provocation, indicating that genetic polymorphisms of EMID2 could cause meaningful deficits in the upper and lower airways among AIA patients. These findings provide evidence that EMID2 may be a susceptible genetic factor for aspirin hypersensitivity among asthmatics in Korean population.

Association analysis of RGS7BP gene polymorphisms with aspirin intolerance in asthmatic patients.

BACKGROUND: Signal-regulated palmitoylation of RGS7BP(regulator of G-protein-signaling 7-binding protein) initiates the activation of G-protein-coupled receptors (GPCRs), including muscarinic receptors, which contribute to the development of asthma and its subphenotypes. OBJECTIVE: To determine the association of RGS7BP gene polymorphisms with the development of aspirin-exacerbated respiratory disease (AERD). METHODS: We evaluated the association of RGS7BP gene polymorphisms with response to oral aspirin challenge and with responsiveness to methacholine challenge. RGS7BP messenger RNA splice variants in peripheral blood platelets from patients with different single-nucleotide polymorphisms were analyzed by reverse-transcription polymerase chain reaction. RESULTS: Logistic regression analysis of RGS7BP gene polymorphisms in patients with AERD (n = 102) and aspirin-tolerant asthma (n = 429) revealed that a haplotype of block 3 consisting of rare alleles +98092 C>G, +98853 C>T, and +104450 T>G of the RGS7BP gene was associated with AERD. Multiple linear regression analysis showed that asthmatic patients carrying ht2/ht2 in block 3 were more responsive to aspirin challenge than those not carrying ht2 (P = .008 in a codominant model). The log-transformed provocation concentration that caused a decrease in forced expiratory volume in 1 second of 20% for methacholine was significantly dependent on the BL3-ht2 haplotype. No significant differences in platelet expression of different RGS7BP messenger RNA splice variants were detected between those with and without the BL3-ht2 haplotype. CONCLUSION: BL3-ht2 of RGS7BP may be an important genetic variant associated with AERD. The haplotype of block 3 may play a protective role against aspirin hypersensitivity in asthma, perhaps by altering the responsiveness of muscarinic receptors.

Current status of Oriental medicine in treating Korean allergy patients.

PURPOSE: To evaluate the prevalence, compliance, pattern of use, and economic cost of OM in Korean allergy patients. METHODS: A total of 647 allergy patients were enrolled from 10 general hospitals, and were surveyed by the questionnaire. It consisted of 12 items and regarded the prescription rates, reasons for referring, their opinions for the efficacy of OM, and economic costs. RESULTS: A total of 259 (40.5%) patients had used OM, and 35.5% of these patients experienced two or more kinds of these practices. A patients' income or education level did not affect the prescription rates of OM. Of the patients that used OM, 34.6% of them were satisfied with the effect of OM treatment, and 40.9% of them were inclined to continue with their OM treatments. The most frequent reasons for choosing OM were the patient's belief that OM can predispose 'allergic constitution to normal' (30.2%), worries about the possible adverse reactions of the long-term administration of the proven drugs (20.2%), and the safety of OM (15.6%). However, 18.9% of these patients experienced perceived adverse events to their OM treatment such as skin rashes, gastrointestinal discomfort, and hepatitis. The patients that have used OM spent on average $915 US dollars annually for OM treatment. CONCLUSIONS: Many Korean allergy patients are cliental to OM. Some patients experienced a satisfactory treatment effect from OM, however, others had no treatment effect, even adverse event. Therefore, it is important to educate people to use OM appropriately to make harmony with modern medicine.

Allergenicity of recombinant troponin C from Tyrophagus putrescentiae.

BACKGROUND: The storage mite, Tyrophagus putrescentiae, produces potent allergens, many of which have not been characterized. This study was undertaken to characterize the allergenicity of troponin C from T. putrescentiae. METHODS: A cDNA encoding 17.7 kDa troponin C, with homology to cockroach allergen Bla g 6, was identified from T. putrescentiae-expressed sequence tags. Recombinant troponin C was expressed and IgE responses to the recombinant protein were assessed in the presence and absence of 10 mM CaCl(2). Cross-reactivity between T. putrescentiae troponin C and Bla g 6 was tested using an inhibition ELISA. RESULTS: Recombinant T. putrescentiae troponin C shares 62.7-85.5% homology with troponin C from various arthropods. Sera from 5 of 47 subjects in our study group (10.6%) showed IgE binding to the recombinant protein. Interestingly, addition of 10 mM CaCl(2) increased the intensity of IgE binding approximately 2-fold. In an immune-inhibition ELISA with these sera, T. putrescetiae troponin C and Bla g 6 did not cross-react significantly. CONCLUSIONS: Troponin C is a new mite allergen with calcium-dependent IgE reactivity.

Tissue transglutaminase can be involved in airway inflammation of toluene diisocyanate-induced occupational asthma.

BACKGROUND: This study was conducted to evaluate whether tissue transglutaminase (tTG) may be involved in airway inflammation of toluene diisocyanate-induced occupational asthma (TDI-OA). METHODS: We enrolled 93 patients with TDI-OA, 177 asymptomatic exposed subjects, 43 patients with allergic asthma, and 70 unexposed normal controls. The prevalence of serum immunoglobulin G (IgG) to tTG in the TDI-OA group (20.2%) was significantly higher than that in the three other groups (P < 0.001). RESULTS: TDI-OA patients with serum IgG to tTG had significantly lower methacholine PC(20) values (P < 0.02) and significantly higher prevalence of specific immunoglobulin E to vapor type TDI-human serum albumin conjugate (P < 0.01; r(2) = 0.411, P < 0.05). TDI exposure could increase tTG activity via reactive oxygen species (ROS) production, which was found to cross-link with cytokeratin 19 on immunoblot analysis. CONCLUSION: Therefore, TDI exposure may activate tTG via ROS-mediated mechanism in the airway epithelium leading to persistent airway inflammation in TDI-OA patients.

Sequence diversity of the Bla g 4 cockroach allergen, homologous to lipocalins, from Blattella germanica.

BACKGROUND: The cockroach allergen Bla g 4, a putative lipocalin, is known to exhibit frequent sequence variations. However, the previously reported cDNA sequences are truncated at the N terminus. This study was undertaken to investigate the mechanisms by which these sequence variations are generated. METHODS: Rapid amplification of cDNA ends PCR and RT-PCR were performed to obtain the full sequence of the Bla g 4 cDNA, and PCR was also used to clone the Bla g 4 genomic DNA. In addition, Bla g 4 protein variants were analyzed by two-dimensional gel electrophoresis. RESULTS: Nine additional amino acid residues at the N terminus of Bla g 4 were identified, and 2 genes encoding Bla g 4, both of which consisted of 5 exons, were cloned. Examination of 34 clones of Bla g 4 cDNA obtained by RT-PCR revealed 14 variants. In particular, Bla g 4 sequences showed frequent clusters of variations in residues 38-45, 61-82 and 144-163. Differences in cDNA sequences may imply that RNA sequences are edited after transcription. More than 10 spots were identified between pH 5 and 7 upon two-dimensional gel electrophoresis, indicating that multiple variants of Bla g 4 are produced at the protein level. CONCLUSIONS: Genetic polymorphisms among individual cockroaches, the existence of multiple genes and sequence variations caused by RNA editing produce sequence diversity of Bla g 4, which may influence its allergenicity. The sequence information obtained in this study will be helpful for the standardization of the cockroach allergen and thereby aid in the development of diagnostics and immunotherapeutics.

Allergenicity of sigma and delta class glutathione S-transferases from the German cockroach.

BACKGROUND: Cockroach glutathione S-transferases (GSTs) are known to elicit strong IgE responses. This study was undertaken to compare the IgE reactivity of German cockroach GSTs, Bla g 5 (sigma class) and delta class GST (BgGSTD1). METHODS: Full-length Bla g 5 and BgGSTD1 were cloned, and their recombinant proteins were expressed and purified. Their IgE reactivities and cross-reactivities were examined by ELISA using sera from cockroach-sensitized subjects. RESULTS: A predominant variant of Bla g 5 cDNA has amino acid substitutions at positions 10 (C to F) and 42 (N to K). BgGSTD1 has substitutions at positions 27 (E to N) and 207 (K to R). Sera from cockroach-sensitized patients showed 20.5% IgE reactivity to Bla g 5 and 17.9% IgE reactivity to BgGSTD1. However, inhibition studies using 1 serum sample with the highest IgE reactivity showed limited cross-reactivity. CONCLUSIONS: IgE-binding frequency to the cockroach GSTs was low, but the titer of IgE reactivity was strong in some sera. The inclusion of different classes of GSTs could be helpful for the delicate diagnosis and immunotherapy of cockroach allergy.

The HLA DRB1*1501-DQB1*0602-DPB1*0501 haplotype is a risk factor for toluene diisocyanate-induced occupational asthma.

BACKGROUND: Although the pathogenesis of toluene diisocyanate (TDI)-induced occupational asthma (TDI-OA) is incompletely understood, several studies have suggested immunologic mechanisms, including specific IgE responses. A few studies have suggested human leukocyte antigen (HLA) associations with TDI-induced asthma in Western countries, but this is the first investigation of associations between HLA class I and II alleles and TDI-induced asthma patients in Asia, using high-resolution analysis. METHODS: Patients with TDI-OA (n = 84), asymptomatic exposed controls (AECs, n = 47) and unexposed normal controls (NCs, n = 127) were enrolled. HLA class I and II genotyping was performed by the direct DNA sequencing analysis. Specific serum IgE antibodies to the vapor type TDI-albumin conjugate were measured by ELISA. RESULTS: There was no significant association between the allele frequencies and the phenotype of TDI-OA. However, the frequency of the HLA DRB1*1501-DQB1*0602-DPB1*0501 haplotype was significantly higher in TDI-OA patients (19%) than in AEC (2.1%, p = 0.007, OR 4.429, CI 1.497-13.103) or NC (3.1%, p < 0.001, OR 7.235, CI 2.236-22.510) subjects, with statistical significance persisting after correction for multiple comparisons. DQB1*0402 was significantly associated with the presence of specific IgE to TDI-albumin conjugates in serum (p = 0.006, OR 4.552, CI 1.540-13.449). This p value remained significant after correction for multiple comparison. CONCLUSION: The HLA DRB1*1501-DQB1*0602-DPB1*0501 haplotype may be a genetic marker for the development of TDI-induced asthma in Koreans. Several HLA alleles that enhance specific IgE sensitization in exposed subjects are indicated.

Spontaneous reporting of adverse drug events by Korean regional pharmacovigilance centers.

PURPOSE: Patterns of prescriptions are markedly influenced by regional disease entities, medical education, culture, economic status, and available pharmaceutical companies. Features of adverse drug reactions (ADRs) may vary in different countries. In this study, we analyzed the causative drugs and clinical manifestations of spontaneously reported ADRs in Korea. METHODS: Six Korean Regional Pharmacovigilance Centers collected 1418 cases of spontaneously reported adverse drug events (ADEs) by doctors, pharmacists, and nurses, and the clinical features and causative drugs were evaluated. The data were collected from general hospitals (76.5%), primary clinics, and pharmacies (23.5%). RESULTS: Based upon the World Health Organization (WHO)-Uppsala Monitoring Center criteria (certain-13.7%, probable-46.1%, possible-32.1%), 91.9% of the collected events were suspected to be ADRs and 15.8% of patients experienced serious ADRs. The most prevalent causative drugs were antibiotics (31.6%), followed by contrast dyes (14.0%), non-steroidal anti-inflammatory drugs (NSAIDs) (11.1%), anti-psychotics (5.4%), anti-convulsants (5.2%), cardiovascular agents (4.8%), anti-neoplastics (4.6%), and opiates and non-opiate pain killers (3.5%). Among the antibiotics, cephalosporins (8.1%) were the most common, followed by anti-tuberculosis agents (5.7%), quinolones (4.0%), vancomycin (3.1%), and penicillin (2.8%). The most common side effect was skin manifestations, which were seen in 42% of the patients, followed by neurologic manifestations (14%), gastrointestinal involvements (12.9%), generalized reactions (9.4%), and respiratory involvements (4.5%). CONCLUSION: Antibiotics, contrast dyes, and NSAIDs were the most common causative drugs for ADRs, which reflects the prescription pattern and the prevalence of diseases in Korea. These data may be useful in establishing a Korean pharmacovigilance system.

IgE binding reactivity of peptide fragments of Bla g 4, a major German cockroach allergen.

Cockroaches have been recognized as a major cause of asthma. Bla g 4 is one of the most important German cockroach allergens. The aim of this study is to investigate IgE reactivity to the recombinant Bla g 4 (rBla g 4) in the sera of allergic patients and identify linear IgE binding epitope. For protein expression, full-length Bla g 4 (EF202172) was divided into 5 overlapping peptide fragments (E1: aa 1-100, E2: aa 34-77, E3: aa 74-117, E4: aa 114-156, and E5: aa 153-182). The full-length and 5 peptide fragments of Bla g 4 was generated by PCR and over-expressed in E. coli BL21 (DE3). The IgE binding reactivities of the full-length and peptide fragments were measured by ELISA using 32 serum samples of cockroach allergy. The sera of 8 patients (25%) reacted with rBla g 4. Four sera (100%) showed IgE-binding reactivity to full-length and peptide fragment 4, and 2 sera (50%) reacted with peptide fragment 2. One (20%) serum reacted with peptide fragment 3. The results of ELISA using overlapping recombinant fragments indicated that the epitope region was located at amino acid sequences 34-73 and 78-113, and major IgE epitope of Bla g 4 was located at amino acid sequences 118-152 of C-terminal. B-cell epitope analysis of German cockroach allergen Bla g 4 could contribute to the strategic development of more specific and potentially efficacious immunotherapy.

Sequence polymorphisms of major German cockroach allergens Bla g 1, Bla g 2, Bla g 4, and Bla g 5.

BACKGROUND: The allergenicity of allergens could be influenced by amino acid substitutions in B- or T-cell epitope regions. The German cockroach is known to produce potent allergens inducing strong IgE-mediated allergic reactions. This study was performed to investigate sequence variations in major allergens of the German cockroach. METHODS: Reverse transcriptase PCR was used to amplify the cDNA sequences encoding major allergens of the German cockroach (Bla g 1, Bla g 2, Bla g 4, and Bla g 5). RESULTS: The deduced amino acid sequences revealed 38 Bla g 1 variants with 1-7 amino acid substitutions (98.6-99.8% identity), 28 Bla g 2 variants with 1-3 substitutions (99.1-99.7%), 27 Bla g 4 variants with 0-32 substitutions (82.4-100%), and 8 Bla g 5 variants with 1-2 substitutions (99.0-99.5%), respectively. Bla g 1 and Bla g 2 showed sporadic amino acid substitutions despite the divergence in their sequences. Bla g 4 exhibited frequent variations, with clusters of substitutions in residues 29-38, 52-80, and 132-155. Sequence variations in Bla g 4 imply the presence of multiple isoforms and isoallergens, which may in turn have various effects on the IgE-binding capacity and T-cell responsiveness. Only 8 variants were found in Bla g 5, with infrequent amino acid changes of one or two residues. CONCLUSIONS: Analyses of T-cell and IgE-binding epitope regions would clarify the effect of sequence polymorphisms on allergenicity, which in turn will aid in the design of allergen formulations for diagnosis and immunotherapy for cockroach allergies.

Characterization of buckwheat 19-kD allergen and its application for diagnosing clinical reactivity.

BACKGROUND: The 19-kD protein of buckwheat (BW) has been suggested to be a major allergen, but its characteristics and clinical significance are poorly defined. METHODS: cDNA of the 19-kD BW allergen was cloned and expressed in Escherichia coli. Allergenicity and cross-allergenicity were confirmed by inhibition immunoblotting or by ELISA inhibition. The recombinant (r19-kD) protein was assessed for clinical utility in the diagnosis of BW reactivity in 18 BW-allergic and 19 BW-asymptomatic sensitized subjects using receiver operating characteristic analysis. RESULTS: The 19-kD BW allergen, which is composed of 135 amino acids, has a weak homology to the vicilin-like allergens of cashew (Ana o 1), English walnut (Jug r 2) and 7 S globulin from Sesamum indicum. The r19-kD protein can inhibit sIgE binding to native 19-kD BW allergen. The maximum percentage inhibition of sIgE binding to crude BW extract was 56%. About 83.3% of the BW allergy patients had sIgE bound to r19-kD protein, compared to only 1 of the 19 BW-asymptomatic sensitized subjects. The areas under the receiver operating characteristic curves for the skin prick tests [0.925 (95% confidence interval: 0.839-1.012), p < 0.001] as well as r19-kD protein sIgE ELISAs [0.860 (95% confidence interval: 0.725-0.995), p <0.001] were higher than that of BW sIgE coated allergen particle test results [0.803 (95% confidence interval: 0.661-0.945), p = 0.002]. CONCLUSIONS: The 19-kD BW allergen may be the major allergen from BW. For the diagnosis of clinical reactivity to BW, the r19-kD protein sIgE ELISA test was more discriminative than the coated allergen particle sIgE measurement using whole BW extract.

Detection and quantification of pharaoh ant antigens in household dust samples as newly identified aeroallergens.

BACKGROUND: The widespread house ant, Monomorium pharaonis (pharaoh ant, PA), was recently identified as a potential cause of respiratory allergies. However, there are no reports of the distribution of PA allergens in various environments. We developed specific ELISA inhibition assays and measured the distribution and amount of PA antigens in household dust samples. METHODS: Floor dust was collected at 3-month intervals from 56 homes in Seoul over a 1-year period. PA antigens in fine dusts were quantified by ELISA inhibition assays using rabbit anti-PA sera, and specific IgE to PA antigens in residents' serum was measured by ELISA. RESULTS: In 18 of the 56 homes (32.1%), PA antigen was detected in at least 1 floor dust sample either from the living room or the kitchen. Levels of PA antigens showed seasonal variations with peaks in autumn and winter. The detection rate of PA antigens was significantly higher in homes with visual evidence of PA infestations (70%) than in homes without such infestations (23.9%; p < 0.05). However, a significant amount of PA antigens was still detected in uninfested homes. Thirteen of 113 (11.5%) residents were positive for PA-specific IgE. PA-specific IgE was detected more frequently in residents living in PA antigen-positive homes (19.6%) than in antigen-negative homes (4.8%; p < 0.05). CONCLUSION: A considerable level of PA antigens is distributed in the indoor environment. Therefore, inhalant exposure to PA antigens can occur during domestic activities. These results suggest that PAs might be a significant source of aeroallergens in households.

Allergy to miscellaneous household arthropods.

Of the various arthropods, humans have the greatest contact with mites and cockroaches, and as a result, allergies to these two groups have been the most frequently reported. Changes in lifestyle and living environment have encouraged the growth of arthropods other than mites and cockroaches, and consequently, human exposure to antigens derived from the new arthropods has increased. Although systematic approaches to and immunobiochemical studies of these arthropods are relatively sparse compared with those of mites and cockroaches, recent reports have shown that many species of household arthropods can elicit IgE-mediated reactions via inhalation, biting, or stinging. In this chapter, we review the other arthropods that can induce allergic reaction to human beings. Where the information exists, the frequency of sensitivity and clinical manifestation, and the characterization of the allergens are also reviewed. Virtually all species of arthropods may be sources of allergens that can sensitize and induce IgE-mediated allergic reactions in humans.

Domestic arthropods and their allergens.

Allergy prevalence has increased worldwide over the last 25 years along with industrialization and westernized lifestyles. Indoor allergens are primarily responsible for the sensitization and development of atopic diseases. The main indoor allergens are known to be derived from various arthropods which account for up to 80% of the kingdom Animalia. The two classes of arthropods are Insecta, which includes cockroaches, flies, mosquitoes, ants and silverfishes, and Arachnida, which includes mites, spiders, ticks, and scorpions and are the main sources of the allergens. Excreted materials, cast-overs from skin-molting, and dead debris are sources of allergens that can sensitize genetically predisposed individuals and elicit allergic disorders. The use of molecular biology techniques has contributed to the identification and characterization of an ever-increasing number of allergens. However, key determinants and allergen properties that drive allergic responses are poorly understood. The biological characterization of allergens will provide an understanding of the pathogenesis of allergic diseases and contribute to the development of new diagnostic and therapeutic approaches.