title: Rapamycin protects kidney against ischemia reperfusion injury through recruitment of NKT cells.
abstract: BACKGROUND
  NKT cells play a protective role in ischemia reperfusion (IR) injury, of which the trafficking in the body and recruitment in injured organs can be influenced by immunosuppressive therapy. Therefore, we investigated the effects of rapamycin on kidneys exposed to IR injury in early stage and on trafficking of NKT cells in a murine model.
  
  
  METHODS
  Balb/c mice were subjected to kidney 30 min ischemia followed by 24 h reperfusion. Rapamycin (2.5 ml/kg) was administered by gavage daily, starting 1 day before the operation. Renal function and histological changes were assessed. The proportion of NKT cells in peripheral blood, spleen and kidney was detected by flow cytometry. The chemokines and corresponding receptor involved in NKT cell trafficking were determined by RT-PCR and flow cytometry respectively.
  
  
  RESULTS
  Rapamycin significantly improved renal function and ameliorated histological injury. In rapamycin-treated group, the proportion of NKT cells in spleen was significantly decreased but increased in peripheral blood and kidney. In addition, the CXCR3+ NKT cell in the kidney increased remarkably in the rapamycin-treated group. The chemokines, CXCL9 and CXCL10, as the ligands of CXCR3, were also increased in the rapamycin-treated kidney.
  
  
  CONCLUSIONS
  Rapamycin may recruit NKT cells from spleen to the IR-induced kidney to ameliorate renal IR injury in the early stage.
authors.forename: Chao
authors.initials: C
authors.lastname: Zhang
authors.forename: Long
authors.initials: L
authors.lastname: Zheng
authors.forename: Long
authors.initials: L
authors.lastname: Li
authors.forename: Lingyan
authors.initials: L
authors.lastname: Wang
authors.forename: Liping
authors.initials: L
authors.lastname: Li
authors.forename: Shang
authors.initials: S
authors.lastname: Huang
authors.forename: Chenli
authors.initials: C
authors.lastname: Gu
authors.forename: Lexi
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Urology, Zhongshan Hospital, Fudan University, Shanghai, China. esuperyc@163.com.
authors.forename: Cheng
authors.initials: C
authors.lastname: Yang
authors.forename: Tongyu
authors.initials: T
authors.lastname: Zhu
authors.forename: Ruiming
authors.initials: R
authors.lastname: Rong
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D019610:Cytoprotection / Q000187:drug effects*; D007511:Ischemia / Q000188:drug therapy* / Q000276:immunology; D007668:Kidney / Q000098:blood supply* / Q000187:drug effects* / Q000276:immunology; D007677:Kidney Function Tests; D007694:Killer Cells, Natural / Q000187:drug effects / Q000502:physiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D015427:Reperfusion Injury / Q000276:immunology / Q000517:prevention & control*; D020123:Sirolimus / Q000627:therapeutic use*
chemical_list: D020123:Sirolimus