Japanese Asthmatic Patients Research Articles

MHC class II restriction for T cell proliferative response to mite antigen.

We investigated the immunoreguratory role of the major histocompatibility complex in peripheral blood lymphocytes' proliferative response to mite antigen. Peripheral blood lymphocytes of Japanese asthmatic patients were incubated with antigen obtained from Dermatophagoides pteronyssinus with a molecular weight of about 15,000, with and without 0.05 microgram/mL of monoclonal antibody against HLA class I or class II for seven days at 37 degrees C humidified in 5% CO2 and 95% air. High and low responders to the mite body antigen were found among the patients while there were no high responders among the healthy individuals tested. In the mite-sensitive asthmatic patients, CD4+ T cells were the population that responded to the antigen. Depletion of CD8+ T cells from the peripheral blood lymphocytes of mite-insensitive individuals caused high responsiveness to the antigen, indicative that the mite-specific CD4+ T cells controlled the high responsiveness and the antigen-specific CD8+ T cells, the low responsiveness. Anti-HLA-DR monoclonal antibody inhibited responsiveness. In contrast, anti-HLA-DQ monoclonal antibody produced high responsiveness in low responders to mite antigen. High T cell proliferative responsiveness to mite antigen was restricted by HLA-DR antigen through CD4+ T cells in high responders, whereas HLA-DQ antigen is a restriction antigen of low responsiveness through CD8+ T cells in low responders and non-atopic individuals.

Intravenous injection of acetaldehyde but not ethanol induces histamine-mediated bronchoconstriction in guinea pigs.

Recently ethanol-induced bronchoconstriction associated with elevated serum levels of acetaldehyde and histamine was reported in Japanese asthmatic patients, but there is no investigation of the airway response to intravenous injection of acetaldehyde. We therefore performed a study in guinea pigs to test the hypothesis that intravenous injection of acetaldehyde has bronchospastic action via histamine release. At first, we investigated the airway response to increasing doses (8.0, 26.4, and 80 mg/ml) of injected ethanol or acetaldehyde in guinea pigs. Secondarily, increasing doses of acetaldehyde were injected in guinea pigs pretreated with an intraperitoneal injection of 20 mg/kg diphenhydramine or saline (control). Finally, injection of acetaldehyde was performed after intraperitoneal injection of 0.5 mg/kg atropine sulfate or saline (control). Injected acetaldehyde caused bronchoconstriction in a dose-dependent manner, but ethanol did not. The bronchoconstriction induced by injected acetaldehyde was completely prevented by pretreatment with diphenhydramine. Atropine had no preventing effect against the acetaldehyde-induced bronchoconstriction. In conclusion, intravenous injection of acetaldehyde causes bronchoconstriction via histamine release in guinea pigs.

Aerosolized acetaldehyde, but not ethanol, induces histamine-mediated bronchoconstriction in guinea-pigs.

It was reported that ethanol-induced bronchoconstriction was associated with elevated serum levels of acetaldehyde and histamine in Japanese asthmatic patients, but there is no study to investigate the airway response to acetaldehyde. We performed this animal study to test the hypothesis that acetaldehyde has the bronchospastic action via histamine release. First, we investigated the airway response to ascending doses (31.3, 62.5, 125, and 250 mM) of inhaled ethanol or acetaldehyde in guinea-pigs. Secondly, guinea-pigs pretreated with intraperitoneal injection of saline or 20 mg/kg diphenhydramine inhaled acetaldehyde. Finally, guinea-pigs pretreated with intraperitoneal injection of saline or 0.5 mg/kg atropine sulfate inhaled acetaldehyde. Inhalation of acetaldehyde, but not ethanol, caused bronchoconstriction in a dose-dependent manner. The bronchoconstriction induced by inhaled acetaldehyde was completely prevented by pretreatment with diphenhydramine. Atropine had no preventing effect against the acetaldehyde-induced bronchoconstriction. In conclusion, acetaldehyde has the bronchospastic action via histamine release in guinea-pigs. It is suggested that histamine H1-antagonists may be available for preventing alcohol-induced asthma.

Specificity concepts in Japan.

In this study, the authors discuss whether there are any differences in the acquired factors, such as psychosocial factors, related to the age at the onset of psychosomatic disorders, and whether or not there are any characteristics which can be considered unique to Japanese asthmatic patients. Many firstborns were found in those whose onset age was below 10 or in their teens. In those patients who had the onset of asthma in their 20s or 30s many women suffered problems with their mother-in-law after marriage or with their husbands who were interested only in work. We have also discussed that behind these phenomena, problems of parent-child relationship in early childhood were hidden.