2002 Fiscal Year Final Research Report Summary
Modulation of Inflammatory Process in COPD Airways
| Project/Area Number |
12470132
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Respiratory organ internal medicine
|
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
ICHINOSE Masakazu Tohoku University, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (80223105)
|
|---|
| Project Period (FY) |
2000 – 2002
|
| Keywords | COPD / nitric oxide / inducible nitric oxide aynthase / peroxynitrite / chronic bronchitis / emphysema / reactive nitrogen / airway inflammation |
|---|
| Research Abstract |
Reactive nitrogen species (RNS) including peroxynitrite and nitrogen dioxide, which are formed in the reaction of nitrogen oxide (NO) with superoxide anion and peroxidase-dependent mechanisms, have a potent inflammatory action. Therefore, these molecules may increase and have a role in inflammatory airway diseases. In the present study, we quantified the RNS using immunostaining of nitrotyrosine and inducible NO synthase (iNOS) in airway inflammatory cells obtained by the induced sputum technique as well as the exhaled NO concentration in chronic obstructive pulmonary disease (COPD), asthma and healthy subjets (HS). iNOS immunoreactivity observed in the airway inflammatory cells was significantly and similarly higher in COPD and asthma compared with HS, although the exhaled NO levels were elevated in asthma but not in COPD and HS. The nitrotyrosine immunoreactivity in the inflammatory cells was obvious in COPD and to a lesser extent in asthma but not in HS. There was a significant negative correlation between the percent predicted values of forced expiratory volume in one second and the amount of nitrotyrosine formation in COPD but not in asthma and HS. These results suggest that 1)RNS may be involved in the pathobiology of the airway inflammatory and obstructive process in COPD, 2)NO produced in the airways, presumably via iNOS, seems to be consumed by its reaction with superoxide anion and/or peroxidase-dependent mechanisms.
|
