title: Reduction of natural killer and natural killer T cells is not protective in cisplatin-induced acute renal failure in mice.
abstract: OBJECTIVE
  A recent report showed that fractalkine (CX3CL1), which functions as both a potent chemoattractant and adhesion molecule for monocytes and natural killer (NK) cells was significantly increased in cisplatin-induced acute renal failure (CisARF) in mice. Therefore, we developed the hypothesis that increased CX3CL1 expression in CisARF initiates NK cell infiltration in the kidney. The aim of the present study was to determine the role of NK cells in CisARF in mice.
  
  
  METHODS
  Time course of pan-NK positive cells in CisARF was investigated by using immunohistochemistry (IHC) for CD49b. Pan-NK positive cells were reduced by using anti-NK1.1 mAb. The model of pan-NK positive cells reduction was confirmed by flow cytometry of the spleen and IHC of the kidney. The expression of granzyme A and caspase-1 was examined, and the activity of caspase-1 was also determined. We performed a study on whether there was significant protection of renal function after reduction of pan-NK positive cells.
  
  
  RESULTS
  (i) Infiltration of pan-NK positive cells was prominent on day 3 after cisplatin administration. (ii) granzyme A expression was significantly increased in CisARF and CisARF+NK1.1 Ab compared to vehicle. (iii) Caspase-1 expression and activity was significantly increased in CisARF mice compared to vehicle and CisARF+NK1.1 Ab. (iv) Reduction of pan-NK positive cells was not protective in cisplatin-induced acute renal failure in mice.
  
  
  CONCLUSIONS
  Although infiltration of pan-NK cells was significantly increased in CisARF, reduction of infiltration of pan-NK cells into the kidney was not protective against CisARF in mice.
authors.affiliation: Department of Laboratory Medicine, Chung-Ang University College of Medicine, Seoul, Korea.
authors.forename: Hye-Ryoun
authors.initials: HR
authors.lastname: Kim
authors.forename: Mi-Kyung
authors.initials: MK
authors.lastname: Lee
authors.forename: Ae-Ja
authors.initials: AJ
authors.lastname: Park
authors.forename: Eon-Seob
authors.initials: ES
authors.lastname: Park
authors.forename: Dong-Seok
authors.initials: DS
authors.lastname: Kim
authors.forename: Jihyun
authors.initials: J
authors.lastname: Ahn
authors.forename: Jaetack
authors.initials: J
authors.lastname: Kim
authors.forename: Su-Hyun
authors.initials: SH
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 / Q000517:prevention & control*; D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D000950:Antigens, Ly / Q000276:immunology*; D017209:Apoptosis; D020170:Caspase 1 / Q000378:metabolism; D054428:Chemokine CX3CL1 / Q000378:metabolism; D002634:Chemotaxis, Leukocyte; D002945:Cisplatin; D004195:Disease Models, Animal; D005434:Flow Cytometry; D053804:Granzymes / Q000378:metabolism; D007150:Immunohistochemistry; D007683:Kidney Tubular Necrosis, Acute / Q000139:chemically induced / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D007684:Kidney Tubules / Q000276:immunology* / Q000473:pathology; D007694:Killer Cells, Natural / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D055651:NK Cell Lectin-Like Receptor Subfamily B / Q000276:immunology*; D051920:NK Cell Lectin-Like Receptor Subfamily D / Q000378:metabolism; D055611:Natural Killer T-Cells / Q000276:immunology*; D013997:Time Factors
chemical_list: D000911:Antibodies, Monoclonal; D000950:Antigens, Ly; D054428:Chemokine CX3CL1; C515539:Cx3cl1 protein, mouse; C527211:Klrb1c protein, mouse; D055651:NK Cell Lectin-Like Receptor Subfamily B; D051920:NK Cell Lectin-Like Receptor Subfamily D; D053804:Granzymes; D020170:Caspase 1; D002945:Cisplatin