No abstract available.
Angioedema* ; Angioedemas, Hereditary* ; Complement C1 Inhibitor Protein* ; Complement C1s*

No abstract available.
Asthma*

No abstract available.

To evaulate the possible pathogenetic significance of allergen-specific IgA antibody in respiratory secretion from asthmatics, we measured house dust mite(HDM)-specific IgA antibody in 3% saline-induced sputum from 23 HDM-sensitive asthmatics, 4 atopic asthmatics without mite-sensitivity, 6 non-atopic asthmatics, and 13 non-atopic, non-asthmatic controls (including 6 non-atopic healthy controls, 4 patients with chronic bronchitis, and 3 patients with rheumatoid arthritis) by ELISA. We also measured HDM-specific IgA antibody in serum and numbers of eosinophils in sputum. 1) Levels of HDM-specific IgA antibody in sputum from mite-sensitive asthmatics were significantly higher than those from non-atopic, non-asthmatic controls and non-atopic asthmatics(p<0.05). Levels of HDM-specific IgA antibody in sputum from atopic asthmatics without mite-sensitivity were significantly higher than those from non-atopic, non-asthmatic controls (p<0.05), however HDM-specific IgA/albumin raito was not significantly different between two groups (p>0.05). 2) The ratio of HDM-specific IgA antibody to albumin in sputum was not significantly different in mite-sensitive asthmatics with sputum eosinophila (> or = 5% of 200 counted leukocytes) and those without sputum eosinophilia (p>0.05). 3) The ratio of HDM-specific IgA to albumin in sputum from asthmatics was higher than that of serum. 4) There was no significant correlation of HDM-specific IgA/albumin ratios between serum and sputum (p>0.05). 5) When comparing sputum and saliva samples from 7 mite-sensitive asthmatics, levels of HDM-specific IgA antibody in sputum were significantly higher than those in saliva (p<0.05). In conclusion, HDM-specific IgA anti-body was increased in sputum from HDM-sensitive asthmatics, and it might be locally produced from bronchial mucosa. To evlauate the pathogenetic significance of allergen-specific IgA antibody in respiratory secretion from asthmatics, further studies might be needed.
Bronchitis, Chronic ; Dust* ; Enzyme-Linked Immunosorbent Assay ; Eosinophilia ; Eosinophils ; Humans ; Immunoglobulin A* ; Mucous Membrane ; Saliva ; Sputum*

BACKGROUND: Measurement of allergen-specific IgE antibodies using enzyme-linked immunosorbent assay (ELISA) has been developed and the results were shown to correlate well with those obtained by radioimmunoassay (RIA). However, consensus on the optirnal condition and data expression method for the measurement of allergen-specific IgE using ELISA is still not present. Object: To define the optimal condition for the measurement of allergen-specific IgE using ELISA and to evaluate the accuracy and reproducibility of the results, METHOD: We measured the concentrations of house dust mite-specific IgE antibodies in serum samples by ELISA and RIA method (AlaSTAT, DPC, USA) using standardized Dermatop~hagoides farinae antigen (kindly donated by Allergopharma Joachim Ganzer KG, Reinbek, Germany). RESULTS: Optirnal antigen coating amount was 2 ug/well and optimal serum dilution was 1: 10 for ELISA. The expression of the absolute concentration of house dust mite-specific IgE antibodies within the unknown sample using serial dilutions of samples and standard serum seemed to be more reasonable than the expression of absorbance value at a single serum dilution, because the former method provided better inter-assay variation and correlation with RIA results. The results of specific IgE rneasurement using ELISA significantly correlated with RIA results (r=0.96, p<0.001, n=26). CONCLUSION: These findings suggest that the measurement of allergen-specific IgE antibodies using the ELISA method can be accurate and reliable if optimal assay conditions and standardized data expression are applied.
Antibodies* ; Consensus ; Dust* ; Enzyme-Linked Immunosorbent Assay* ; Immunoglobulin E* ; Pyroglyphidae ; Radioimmunoassay

BACKGROUND: Toluene diisocyanate (TDI) is the most prevalent agent to cause occupational asthma (OA) in Korea. The pathogenic mechanism of TDI-induced OA is still unclear. Involvement of both immunological and non-immunologicaI mechanisms have been suggested. OBJECTIVE: To evaluate a possible role of neutrophil in the development of TDI-asthma. OBJECT AND METHOD: Myeloperoxidase (MPO) as a neutrophil activation marker in both serum and induced sputum, and IL-8 in induced sputum were measured. Induced sputa and sera were collected from 15 TDI-induced OA patients (classified to group I) during TDI- bronchoprovocation test and were compared with those from 11 asthmatic subjects with negative TDI-bronchoprovocation test (group II). MPO levels were measured by radioimmunoassay, IL-8 levels, by enzyme linked immunosorbent assay and albumin levels, by nephelometry. Sputum MPO and IL-8 levels were presented as a ratio to albumin. RESULT: Serum MPO level tended to decrease during the TDI-bronchoprovocation test in two groups, but no statistical significance was reached (p>0.05). However, the ratios of MPO (the ratio of MPO level measured at 30 min to MPO level at baseline, and the ratio MPO level measured at 360 min to MPO baseline) in group I were significantly lower than group II (p=0.004, p=0.03 respectively). The IL-8/albumin and MPO/albumin levels in induced sputum from group I were significantly increased after the TDI-bronchprovocation test in comparison to the baseline value which was obtained before the bronchoprovocation test (p=0.0l, p=0.02 respectively). There was a significant correlation between the percent increase of IL-8/albumin and the MPO/albumin in induced sputum (r=0.89, p<0.05). CONCLUSION: These findings suggest a possible involvement of neutrophil in the development of bronchoconstiction after the TDI exposure, and IL-8 might contribute to neutrophil recruitment to airway mucosa. Further investigation will be needed to investigate mechanism of neutrophil activation in the pathogenesis af TDI-induced OA.
Asthma, Occupational* ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-8 ; Korea ; Mucous Membrane ; Nephelometry and Turbidimetry ; Neutrophil Activation* ; Neutrophil Infiltration ; Neutrophils* ; Peroxidase ; Radioimmunoassay ; Sputum* ; Toluene 2,4-Diisocyanate

Asthma is commonly recognized as a heterogeneous condition with a complex pathophysiology. With advances in the development of multiple medications for patients with asthma, most asthma symptoms are well managed. Nevertheless, 5% to 10% of adult asthmatic patients (called severe asthma) are in uncontrolled or partially controlled status despite intensive treatment. Especially, severe eosinophilic asthma is one of the severe asthma phenotypes characterized by eosinophilia in sputum/blood driven by type 2 immune responses. Eosinophils have been widely accepted as a central effector cell in the lungs. Some evidence has demonstrated that persistent eosinophilia in upper and lower airway mucosa contributes to asthma severity by producing various mediators including cytokines, chemokines and granule proteins. Moreover, extracellular traps released from eosinophils have been revealed to enhance type 2 inflammation in patients with severe asthma. These novel molecules have the ability to induce airway inf lammation and hyperresponsiveness through enhancing innate and type 2 immune responses. In this review, we highlight recent insight into the function of eosinophil extracellular traps in patients with severe asthma. In addition, the role of eosinophil extracellular vesicles in severe asthma is also proposed. Finally, current biologics are suggested as a potential strategy for effective management of severe eosinophilic asthma.

Background/Aims: Sensitization to staphylococcal superantigens (SAgs) could contribute to asthma severity. However, its relevance with eosinophilic phenotype has not yet been clarified. This study aimed to investigate associations between serum specific IgE levels to SAg and eosinophilic airway inflammation in adult asthmatics. Methods: The serum specific IgE levels to 3 SAgs, including staphylococcal enterotoxin A (SEA) and B (SEB), and toxic shock syndrome toxin-1 (TSST-1) were measured by ImmunoCAP in 230 adult asthmatic patients and 50 healthy controls (HCs). Clinical characteristics and laboratory parameters, including serum total/free IgE, and 2 eosinophil-activation markers, eosinophil cationic protein (ECP), and eosinophil-derived neurotoxin (EDN), were analyzed according to blood eosinophil counts (BEC; 150 cells/μL) and serum specific IgE levels to 3 SAgs (0.35 kU/L). Results: Asthmatic patients showed higher serum specific IgE levels to 3 SAgs than HCs (p < 0.05 for all). The serum total/clinfree IgE levels were significantly higher in asthmatics with positive IgE responses to 3 SAgs than those without (p < 0.05 for all). There were no significant differences in clinical parameters including age, asthma severity, comorbidities, or smoking according to IgE responses to 3 SAgs. Patients with positive IgE responses to SEB (not to SEA/TSST-1) had higher serum specific IgE levels to house dust mites and ECP/EDN as well as higher BEC with positive correlations between serum SEB-specific IgE levels and BEC/ECP/EDN (p < 0.05 for all). Conclusions These findings suggest that serum SEB-specific IgE levels could contribute to eosinophil activation as well as IgE production in adult asthma.