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Notes: Background There have been very few reports of occupationai allergies caused by inhalation of buckwheat flour. In this paper, we present a case of occupational asthma and rhinitis caused by buckwheat flour inhalation.Methods and results The patient had strong positive responses to grass and ragweed poiiens as well. The bronchoprovocation test showed early asthmatic response to buckwheat flour extracts. Serum specific IgE antibody to buckwheat flour was detected by enzyme-linked immunosorbent assay (ELISA). In order to further identify the allergenic component of the extracts, sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and electroblotting studies were performed. Eight IgE binding components (9–55 kDa) were detected within the buckwheat flour extracts.Conclusion These results suggest that inhalation of buckwheat flour can caused IgE mediated bronchoconstriction.

Notes: Background Urticaria/angioedema is a common aspirin-induced allergy; however, its pathogenic mechanism is not understood.Objective In order to uncover the genetic mechanism, we studied the associations of the human leucocyte antigen (HLA) genotypes in patients with aspirin-induced urticaria compared with aspirin-intolerant asthma and normal control in a Korean population.Methods Ninety-four aspirin-induced urticaria patients presenting urticaria/angioedema-induced by both ASA and NSAID (50 had underlying chronic urticaria) and showing positive responses on oral aspirin challenge test, 76 aspirin-intolerant asthmatics with positive responses on lysine–aspirin bronchoprovocation test, and 185 normal healthy controls were enrolled. HLA-DRB1, DQB1, and DPB1 genotypings were performed by direct DNA sequencing analysis.Results The allele frequencies of HLA-DRB1*1302 (18.1%) and HLA-DQB1*0609 (10.1%) in aspirin-induced urticaria were significantly higher than in aspirin-intolerant asthma (5.3%, P=0.0004; 2.0%, P=0.0024) and in normal controls (8.1%, P=0.0005; 3.2%, P=0.0008), and they remained significant after correcting for multiple comparisons. The patients with these two HLA markers had a significantly younger age than patients without, while no associations were found in with respect to atopic status, a history of previous allergic diseases, total IgE level, or presence of underlying chronic urticaria (P〉0.05, respectively). In haplotype analysis, the HLA-DRB1*1302-DQB1*0609-DPB1*0201 was significantly higher in the aspirin-induced urticaria (8.0%) than in the aspirin-intolerant asthma (0.7%, P=0.0014) and normal controls (2.0%, P=0.0006).Conclusion These findings suggest that the HLA-DRB1*1302-DQB1*0609-DPB1*0201 may be a strong genetic marker to determine the aspirin-induced urticaria phenotype.

Notes: Background Nasal polyps infiltrated with eosinophils are commonly found in chronic asthmatic patients, more frequently in those with aspirin-intolerant asthma (AIA) than aspirin-tolerant asthma (ATA). Some studies have suggested a contribution of superantigens derived from Staphylococcus sp to nasal polyposis and eosinophilia, but their relative importance in AIA and ATA subjects is unknown.Objective We investigated whether local production of specific IgE to staphylococcal enterotoxins A and B (SEA and SEB) and relationships with markers of eosinophilic inflammation differ in the nasal polyps of AIA and ATA subjects.Methods Fifteen AIA subjects with positive responses to lysine–aspirin bronchoprovocation and 15 ATA subjects underwent polypectomy. Immunoassays were used to quantify eosinophil cationic protein (ECP), IL-5, mast cell tryptase, soluble IL-2 recepters (sIL-2R), total IgE, and specific IgE for SEA and SEB.Results ECP levels in nasal polyp homogenates were higher in AIA subjects than in ATA subjects (P〈0.02), with no significant differences in tryptase, IL-5 or sIL-2R. Total IgE, and specific IgE to both SEA and SEB, were detectable in some nasal polyps from both subject groups, but median levels were markedly higher in AIA subjects than in ATA subjects (P=0.04, 0.01, 0.05, respectively). Levels of specific IgE to SEA and SEB correlated significantly with levels of ECP and IL-5, but not those of tryptase or sIL-2R.Conclusion These findings suggest that staphylococcal superantigens may drive local eosinophilic inflammation in nasal polyp tissue, and that this is exacerbated in subjects with AIA.

Notes: Background Eosinophils are known to be main effector cells in allergic inflammation and IgA antibody has been shown to be a potent stimulus for eosinophil degranulation in in vitro conditions.Objective To evaluate the possible role of IgA antibodies on eosinophil degranulation in lower respiratory mucosa of asthmatics, we tried to find a correlation between total IgA and eosinophil cationic protein (ECP) levels in induced sputum from asthmatics.Methods We measured total IgA and albumin levels by nephelometry, and eosinophil cationic protein levels by Pharmacia CAP system in induced sputum from 23 atopic asthmatics and 12 healthy controls.Results IgA and albumin levels in induced sputum from asthmatics with sputum eosinophilia (sputum eosinophil count 5% of 200 counted non-squamous cells) were significantly higher (P 〈 0.05) than those from controls. However, IgA and albumin levels in induced sputum from asthmatics without sputum eosinophilia were not significantly different with those from controls (P 〉 0.05). In induced sputum from asthmatics, ECP levels were significantly correlated with albumin (r= 0.44, P= 0.04) and IgA levels (r= 0.67, P= 0.002). ECP/albumin ratio was also significantly correlated with IgA/albumin ratio (r= 0.61, P= 0.004).Conclusion Our results support the hypothesis that IgA antibodies in tracheobronchial secretion may be involved in eosinophil degranulation in asthma, and further study is needed to prove this hypothesis.

Notes: Background and objective Persistent asthma symptoms are associated with airway inflammation and remodeling, which may be mediated through metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP). The aim of this study was to evaluate MMPs and TIMP involvement in toluene diisocyanate (TDI)-induced asthma.Materials and method Induced sputum was collected in eight newly diagnosed TDI-induced asthma subjects (group I) before and 7 h after the TDI and placebo challenges and in 12 subjects with TDI-induced occupational asthma diagnosed 5 years previously with persistent asthma symptoms (group II). Sera was collected in group I at diagnosis, and in group II, they were collected at the time of the study. 12 nonasthmatic healthy subjects were enrolled as controls. MMP-9, MMP-2 and TIMP-1 levels in both sputum and serum were measured by enzyme-linked immunosorbent assay (ELISA). Gelatinase activity in the sputum was confirmed by zymographic analysis.Results The serum TIMP-1 level was significantly higher in asthma patients than in healthy controls (P = 0.01), while MMP-9 level was significantly lower in asthmatic patients (P = 0.03). There was no significant difference in MMP-2 level (P = 0.27). MMP-9 level in the sputum was significantly increased after the TDI challenges (P = 0.01). TIMP-1 level in sputum tended to increase after TDI challenges, but no statistical significance was noted (P = 0.09). MMP-9 and MMP-9/TIMP-1 levels in the sputum were significantly higher in group II than in group I (P = 0.04, P = 0.02) with no significant difference in TIMP-1 level. Minimal amount of MMP-2 was found in sputum. Zymography demonstrated that MMP-9 level increased and active form of MMP-9 was generated after the TDI bronchoprovocation test.Conclusion TDI exposure leads to overproduction of MMP-9, which may induce airway inflammation and remodeling, and then contribute to persistent asthmatic symptoms in TDI-induced asthma.

Notes: Background The outcome of isocyanatc-induced occupational asthma remains to be further defined. There have been few studies on the role of specific antibodies in prognosis of toluene diisocyanate (TDI) induced occupational asthma. Moreover, to the best of our knowledge, there have been no studies on the improvement pattern of airway hyper-responsiveness (AH). We analysed the prognostic factors that affected the outcome of 35 toluene diisocyanate-induced occupational asthma.Objectives To define clinical and laboratory parameters predicting favourable prognosis for TDI-induced occupational asthma.Methods and results After confirmation of bronchial sensitivity by TDI hronchoprovocation test (BPT), 35 patients were recommended to avoid exposure to TDI; they were also given anti-asthmatic medications including inhaled steroids and monitored for 2 years. Seventeen (49%) recovered completely with disappearance of airway hyperresponsiveness (AH) to methacholine during the follow-up period (mean duration: 12 months, range of 3–30 months). Eleven (31%) showed a significant improvement in AH for first year, which improvement stabihzed in the next year with mild symptoms. Seven (20%) patients did not show any evidence of improvement in AH and had persistent symptoms. Favourable prognosis was associated with a short duration of asthmatic symptoms before diagnosis (P 〈 0.05), immediate cessation of exposure after diagnosis (P 〈 0.05), milder degree of AH at diagnosis (P 〈 0.05), and the presence of specific IgE antibodies to TDI-human serum albumin conjugate (0.05 〈 P 〈 0.1). No association was found with atopic and smoking status, age, exposure duration, or length of latent period (P 〉 0.05).Conclusion These data suggest that early detection of TDI-induced asthma and immediate cessation of exposure are important factors for a favourable prognosis.

Notes: Background Our previous study reported that more than 50% of toluene diisocyanate (TDI)-induced asthma patients had persistent asthmatic symptoms even after complete avoidance. Although specific IgE (sIgE) has been detected in a portion of patients with TDI-asthma, a recent investigation suggests that the presence of serum specific IgG (sIgG), not sIgE, is more closely associated with positive bronchoprovocation test (BPT) results.Objective To evaluate the possible role of sIgE and sIgG in predicting long-term prognosis of TDI-asthma.Materials and methods Forty-one TDI-asthma patients whose diagnosis was confirmed by TDI-BPT, and 20 unexposed healthy controls were enrolled. Both sIgE and sIgG to TDI-human serum albumin (HSA) conjugate were detected by ELISA. All patients with persistent asthmatic symptoms took anti-asthmatic medications during the follow-up period (mean: 67.5 months) and were instructed to avoid exposure to TDI. Airway hyper-responsiveness to methacholine (AHM) was monitored every year during the study period. The patients were classified into three groups according to changing patterns of AHM and asthmatic symptoms as follows: group I, no improvement with persistent asthmatic symptoms (n = 12); group II, partial improvement with persistent asthmatic symptoms (n = 13); group III, in remission (n = 16).Results Favourable prognosis was associated with a mild degree of AHM at initial diagnosis (P 〈 0.05). Although there were no significant differences in the prevalence of sIgE antibody to TDI-HSA conjugate among the three groups (P 〉 0.05), prevalence of sIgG in group I tended to be higher than in group II (0.05 〈 P 〈 0.1). However, the levels of sIgG were significantly higher in group I than in group II (P = 0.05), whereas levels of sIgE were significantly higher in group II than in group I (P = 0.014). No significant differences were noted in exposure duration, sex, age, atopic status, and total IgE level among the three groups (P 〉 0.05).Conclusion This study confirmed that a favourable outcome is related to a mild degree of AHM and to low levels of sIgG to predict persistent asthmatic symptoms, it also suggested that the presence of high serum-specific IgE at initial diagnosis may represent a better prognosis.

Notes: Background: We report a case of hypersensitivity pneumonitis (HP) in a 17-year-old male student caused by Fusarium napiforme found in his home environment. Methods: The patient was diagnosed according to history, chest radiograph, spirometry, high-resolution chest CT, and transbronchial lung biopsy. To identify the causative agent, cultured aeromolds were collected by the open-plate method. From the main fungi cultured, fungal antigens were prepared, and immunoblot analysis with the patient's serum and each fungal antigen was performed. Results: Five fungal species were isolated from the patient's home. Immunoblotting analysis with the patient's serum demonstrated more than 10 IgG-binding fractions to F. napiforme extract only, while little binding was noted with the other fungal antigens. Conclusions: We should be aware that HP may be caused by F. napiforme in the home environment.

Notes: Background:  5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA). To date, studies of the promoter region of ALOX5 gene has revealed the potential influence of a variable number of tandem repeats of a Sp1- and Egr1-binding motif, on the transcription rate.Methods:  To understand the pathological process that arises from cys-LT overproduction in AIA, we genotyped ALOX5 Sp1 and ALOX5AP poly(A) repeat promoter polymorphism by fluorescent-based capillary electrophoresis in the Korean population.Results:  No significant differences in allele and genotype frequencies of the ALOX5 and ALOX5AP promoter polymorphisms were observed between the three groups. However, there was a strong association of the ALOX5 Sp1 repeat polymorphism with airway hyperresponsiveness (AHR; PC20 methacholine); AIA patients carrying a mutant allele (n 〉 5 or n 〈 5 repeats) showed increased AHR compared to AIA patients with wild-type genotype (P = 0.003).Conclusion:  Although the alleles of the ALOX5 and ALOX5AP promoter cannot be considered as a prominent risk factor in the development of AIA, the genetic variant of tandem repeat (GGGCGG; Sp1-binding motif) in ALOX5 promoter is associated with the severity of airway hyperresponsiveness in AIA patients.