| First Author | Hamaguchi Y | Year | 2002 |
| Journal | Am J Pathol | Volume | 161 |
| Issue | 5 | Pages | 1607-18 |
| PubMed ID | 12414509 | Mgi Jnum | J:79905 |
| Mgi Id | MGI:2389550 | Doi | 10.1016/S0002-9440(10)64439-2 |
| Citation | Hamaguchi Y, et al. (2002) Intercellular adhesion molecule-1 and L-selectin regulate bleomycin-induced lung fibrosis. Am J Pathol 161(5):1607-18 |
| abstractText | The development of bleomycin-induced lung injury, a model of pulmonary fibrosis, results from inflammatory cell infiltration, a process highly regulated by the expression of multiple adhesion molecules. At present, the identity and role of the adhesion molecules involved in the fibrotic process are unknown. Therefore, bleomycin-induced pulmonary fibrosis was examined in mice lacking L-selectin (L-selectin(-/-)) expression, intercellular adhesion molecule-1 (ICAM-1) expression, or both. After 16 days of intratracheal bleomycin challenge, collagen deposition was inhibited in both L-selectin(-/-) and ICAM-1(-/-) mice when compared with wild-type littermates. Interestingly, collagen deposition was virtually eliminated in L-selectin/ICAM-1(-/-) mice relative to either the L-selectin(-/-) or ICAM-1(-/-) mice. Decreased pulmonary fibrosis was associated with reduced accumulation of leukocytes, including neutrophils and lymphocytes. Decreased mRNA expression of proinflammatory cytokines and transforming growth factor (TGF)-beta1 paralleled the inhibition of collagen deposition. The present study indicates that L-selectin and ICAM-1 play a critical role in pulmonary fibrosis by mediating the accumulation of leukocytes, which regulate the production of proinflammatory cytokines and TGF-beta1. This suggests that these adhesion molecules are potential therapeutic targets for inhibiting human pulmonary fibrosis. |
