| First Author | Takahashi N | Year | 1995 |
| Journal | J Appl Physiol (1985) | Volume | 79 |
| Issue | 5 | Pages | 1753-61 |
| PubMed ID | 8594038 | Mgi Jnum | J:30287 |
| Mgi Id | MGI:77800 | Doi | 10.1152/jappl.1995.79.5.1753 |
| Citation | Takahashi N, et al. (1995) Expression of ICAM-1 in airway epithelium after acute ozone exposure in the mouse. J Appl Physiol 79(5):1753-61 |
| abstractText | We investigated the time course and regional distribution of the expression of intercellular adhesion molecule-1 (ICAM-1) on airway epithelial cells and the polymorphonuclear leukocyte (PMN) inflammatory response in the lung after acute exposure to ozone (O3). C57BL/6J mice were exposed to air or 2 ppm O3 for 3 h and killed immediately or 3, 6, 9, or 21 h after exposure. Expression of ICAM-1 was examined by immunohistochemical staining of frozen sections. PMN influx was evaluated by lavage and by histochemical staining of myeloperoxidase (MPO) and measurement of tissue MPO activity. ICAM-1 expression exhibited regional selectivity and temporal patterns that were unique to each region. Upregulation of ICAM-1 expression on the epithelial cells in the trachea, and to a lesser extent in the lobar and segmental bronchi, was observed 3-9 h after exposure and remained present at 21 h. Enhanced ICAM-1 expression in bronchioles and terminal bronchiole/alveolar duct regions was evident earlier (immediately to 3 h after exposure) but returned to baseline levels by 21 and 9 h, respectively. Maximal ICAM-1 expression and PMN influx in the lung parenchyma were concurrently observed at 3 h, followed by transepithelial migration of PMNs to the airway lumen. These results demonstrate regional variations in airway inflammatory activity and are supportive of the notion that upregulation of ICAM-1 on the airway epithelium may play a role in local regulation of PMN influx to the airways after acute O3 exposure. |
