Jinichiro Akiyama

Epigallocatechin Gallate-Induced Histamine Release in Patients with Green Tea-Induced Asthma

BACKGROUND AND OBJECTIVE Epigallocatechin gallate is the causative agent of green tea-induced asthma. To determine whether an IgE-mediated mechanism plays a pathogenetic role in this disorder, we measured histamine release after in vitro exposure to epigallocatechin gallate. METHODS Subjects included eight patients (four men and four women) with green tea-induced asthma, who had been diagnosed by skin test and inhalation challenge, and eight controls (four asthmatic subjects with no previous exposure tea dust and four healthy volunteers). Heparinized whole blood samples were taken and incubated with epigallocatechin gallate at various concentrations (final concentration range, 0.003 to 300 micrograms/mL) for 30 minutes at 37 degrees C. After centrifugation, histamine was measured in the cell-free supernatants by radioimmunoassay. Histamine release was expressed as a percentage of total histamine. A result higher than 10% was considered positive. RESULTS In one of the tea-sensitive patients, epigallocatechin gallate did not cause histamine release. Five of the other seven patients (71%) demonstrated a positive, dose-dependent histamine release to epigallocatechin gallate. In asthmatic and normal controls, histamine release was not observed at any epigallocatechin gallate concentration. Furthermore, a significant correlation was noted between the maximum percentage histamine release and the threshold epigallocatechin gallate concentration for intradermal skin testing. CONCLUSION These results indicate that an IgE-mediated response is the basis for green tea-induced asthma.

The Detection of Two Surface Antigens on Human Lung Macrophages Using Monoclonal Antibodies

Monoclonal antibodies (McAb), designated AMH1 (IgM, lambda) and AMH2 (IgG1, Kappa), against specific surface antigens of human lung macrophages were produced by the fusion of the NS‐1 plasmacytoma cell line with spleen cells from BALB/c mice immunized with bronchoalveolar lavaged (BAL) cells obtained from selected smoking subjects. The screening and characterization of these McAb were carried out employing cellular radioimmunoassay, flow cytofluorography, and immunohistochemical methods. These two antibodies specifically reacted with macrophages in the alveolar spaces and BAL fluids. AMH1 did not react with peripheral blood cells including freshly separated monocytes, cultured monocytes, lymphocytes, granulocytes, and platelets. In addition, AMH1 did not react with peritoneal exudate cells or pleural exudate cells. On the other hand AMH2 showed the dull‐positive reaction with some monocytes and pleural exudate cells among above‐mentioned cells. These two McAb seemed to detect cell surface antigens that are expressed by highly differentiated or mature macrophages compared to OKM1. These antibodies will allow not only better characterization of immune cells but also assessment of maturity of lung macrophages.