| Project/Area Number |
09670603
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Respiratory organ internal medicine
|
|---|
| Research Institution | University of Tokyo |
|---|
Principal Investigator |
MATSUSE Takeshi Univ. of tokyo, Dept. of Geriatric Medicine, Lecturer, 医学部・附属病院, 講師 (90199795)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KATAYAMA Hirofumi Univ. of Tokyo, Dept. of Geriatric Medicine, Medical staff, 医学部・附属病院, 医員
OKA Teruaki Univ. of Tokyo, Dept. ofPathology, Lecturer, 医学部・附属病院, 講師 (60177029)
|
|---|
| Project Period (FY) |
1997 – 1998
|
| Project Status |
Completed (Fiscal Year 1998)
|
| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1997: ¥1,900,000 (Direct Cost: ¥1,900,000)
|
|---|
| Keywords | cigarette / lung inflammation / ICAM-1 / bronchoalveolar lavage / immunohistochemistry / immunohistochemistry / Immunohistochemistry |
|---|
| Research Abstract |
Cigarette smoking induces accumulation of polymorphonuclear leukocytes (PMNs) and mononuclear cells in the peripheral lung. The purpose of this report was to investigate the role of intercellular adhesion molecule-1 (ICAM-1) in a murine model of acute cigarette smoke inhalation-induced lung inflammation. ICR mice were exposed to 100 cigarettes for 2 h pretreated with phosphate buffered saline (Smoke group), an anti-ICAM-1 mAb (ICAMmAb+Smoke group). In the Smoke group, significant increases in total cell, macrophage and PMN counts of bronchoalveolar lavage fluid were observed at 12 h after cigarette smoke exposure. This accumulation of inflammatory cells was significantly reduced by the pretreatment with an anti-ICAM-1 mAb (p<O.O1). Adherence of myeloperoxydase positive PMNs to vascular endothelium and bronchiolar epithelium significantly increased at 12 h after exposure, and this increase of adherent PMNs was attenuated significantly by the pretreatment with anti-ICAM-1 mAb (p<O.O5). The increased expression of ICAM-1 on bronchiolar epithelium was observed after exposure. These observations suggest that the upregulation of ICAM-1 may play an important role in the inflammatory process of airways caused by cigarette smoke inhalation.
|
