| First Author | Nakatani-Okuda A | Year | 2005 |
| Journal | Am J Physiol Lung Cell Mol Physiol | Volume | 289 |
| Issue | 2 | Pages | L280-7 |
| PubMed ID | 15792964 | Mgi Jnum | J:104755 |
| Mgi Id | MGI:3612749 | Doi | 10.1152/ajplung.00380.2004 |
| Citation | Nakatani-Okuda A, et al. (2005) Protection against bleomycin-induced lung injury by IL-18 in mice. Am J Physiol Lung Cell Mol Physiol 289(2):L280-7 |
| abstractText | The role of interleukin (IL)-18 in the protection from interstitial pneumonia and pulmonary fibrosis induced by bleomycin (BLM) was investigated by comparing the severity of BLM-induced lung injuries between wild-type and C57BL/6 mice with a targeted knockout mutation of the IL-18 gene (IL-18-/- mice). IL-18-/- mice showed much worse lung injuries than wild-type mice, as assessed by the survival rate, histological images, and leukocyte infiltration in the bronchoalveolar lavage fluid and myeloperoxidase activity. In wild-type mice, administration of IL-18 before BLM instillation resulted in suppression of lung injuries, increases in the hydroxyproline content, and decreases in the granulocyte-macrophage colony-stimulating factor content in the lung. Preadministration of IL-18 also resulted in prevention of the reduction of the lung IL-10 content caused by BLM-induced damage of alveolar epithelial. BLM instillation suppressed superoxide dismutase (SOD) activity in IL-18-/- mice to a greater extent than in wild-type mice. Pretreatment of IL-18 augmented Mn-containing superoxide dismutase (Mn-SOD) messenger RNA expression and SOD activity in the lung and prevented the reduction of SOD activity caused by BLM in both wild-type and IL-18-/- mice. These results suggest that IL-18 plays a protective role against BLM-induced lung injuries by upregulating a defensive molecule, Mn-SOD. |
