| First Author | Jing W | Year | 2018 |
| Journal | Int Immunopharmacol | Volume | 63 |
| Pages | 1-8 | PubMed ID | 30056257 |
| Mgi Jnum | J:310779 | Mgi Id | MGI:6511370 |
| Doi | 10.1016/j.intimp.2018.07.032 | Citation | Jing W, et al. (2018) G-CSF mediates lung injury in mice with adenine-induced acute kidney injury. Int Immunopharmacol 63:1-8 |
| abstractText | Acute lung injury (ALI) is a serious complication among patients with acute kidney injury (AKI) that is a systemic inflammatory disease with high morbidity and mortality. The pathophysiology of AKI-associated ALI is poorly understood. G-CSF regulates the production and function of neutrophils that mediate lung injury via elastase and other mediators. Here, we used a mouse model of adenine-induced AKI to determine the roles of G-CSF and neutrophil elastase in AKI-associated ALI. We confirmed that ALI was associated with high serum G-CSF levels, and elevated neutrophil elastase activity in the lungs and serum of mice with adenine-induced AKI. Systemic administration of G-CSF-specific neutralizing antibody normalized granulopoiesis, pulmonary neutrophil infiltration, and neutrophil elastase activity, conferring improved lung architecture in mice with adenine-induced AKI. Further studies revealed that macrophages secreted G-CSF upon urea stimulation. Consequently, G-CSF could be a target for new anti-lung injury strategy in patients with AKI. |
