title: Role of IL-1α in cisplatin-induced acute renal failure in mice.
abstract: OBJECTIVE
  For unknown reasons, caspase-1 -/- mice, protected against cisplatin-induced acute renal failure (ARF), are deficient in interleukin (IL)-1α. We thus asked whether IL-1α deficiency underlies the mechanism of protection against cisplatin-induced ARF in these mice.
  
  
  METHODS
  Cisplatin (30 mg/kg) was injected intraperitoneally into wild-type C57BL/6 mice to produce a cisplatin-induced model of ARF. IL-1α was measured in control vehicle- and cisplatin-treated wild-type animals. We also examined whether IL-1α -/- mice were similarly protected against cisplatin-induced ARF. Additionally, infiltration of CD11b- and CD49b-positive cells, as markers of macrophages, natural killer, and natural killer T cells (pan-NK cells), was investigated in wild-type and IL-1α -/- mice.
  
  
  RESULTS
  Compared with vehicle-treated mice, renal IL-1α increased in cisplatin-treated wild-type mice beginning on day 1. IL-1α -/- mice were shown to be protected against cisplatin-induced ARF. No significant difference in the infiltration of neutrophils or CD11b- and CD49b-positive cells were observed between wild-type and IL-1α -/- mice.
  
  
  CONCLUSIONS
  Mice deficient in IL-1α are protected against cisplatin-induced ARF. The lack of IL-1α may explain, at least in part, the protection against cisplatin-induced ARF observed in caspase-1 -/- mice. Investigation of the protective mechanism (s) in IL-1α -/- mice in cisplatin-induced ARF merits further study.
authors.affiliation: Department of Internal Medicine, Chung-Ang University College of Medicine, Seoul, Korea.
authors.forename: Jay-Wook
authors.initials: JW
authors.lastname: Lee
authors.forename: Woo-Jin
authors.initials: WJ
authors.lastname: Nam
authors.forename: Min-Jee
authors.initials: MJ
authors.lastname: Han
authors.forename: Jung-Ho
authors.initials: JH
authors.lastname: Shin
authors.forename: Jin-Gun
authors.initials: JG
authors.lastname: Kim
authors.forename: Su-Hyun
authors.initials: SH
authors.lastname: Kim
authors.forename: Hye-Ryoun
authors.initials: HR
authors.lastname: Kim
authors.forename: Dong-Jin
authors.initials: DJ
authors.lastname: Oh
mesh_terms: D058186:Acute Kidney Injury / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D000818:Animals; D017209:Apoptosis; D015415:Biomarkers / Q000097:blood; D001806:Blood Urea Nitrogen; D039481:CD11b Antigen / Q000032:analysis; D002945:Cisplatin; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D005455:Fluorescent Antibody Technique; D039421:Integrin alpha2 / Q000032:analysis; D053582:Interleukin-1alpha / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D007668:Kidney / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D007694:Killer Cells, Natural / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D055611:Natural Killer T-Cells / Q000276:immunology; D009336:Necrosis; D020556:Neutrophil Infiltration; D013997:Time Factors
chemical_list: D015415:Biomarkers; D039481:CD11b Antigen; D039421:Integrin alpha2; D053582:Interleukin-1alpha; D003404:Creatinine; D002945:Cisplatin