title: Ischemia-reperfusion injury activates innate immunity in rat kidneys.
abstract: BACKGROUND
  There is growing evidence of a role of the immune system in the pathophysiology of ischemia-reperfusion (I/R) injury, but the influence of I/R injury on innate immunity is still undetermined.
  
  
  METHODS
  Sprague-Dawley rats were used. I/R injury was induced by clamping both renal arteries for 45 min, and the rats were killed 1, 3, 5, and 7 days later. Activation of innate immunity was evaluated in terms of the expression of toll-like receptor (TLR) 2 or TLR4 mRNAs and protein, by the level of the TLR ligand (heat shock protein [HSP] 70), and maturation of dendritic cells by double-label immunohistochemistry of dendritic cells for major histocompatibility complex (MHC) class II antigen.
  
  
  RESULTS
  I/R injury increased TLR2 and TLR4 mRNA and protein expression, and they were mainly observed on renal tubular cells. I/R injury also produced endogenous TLR ligand (HSP70) on renal tubular cells. I/R injury increased not only the numbers of dendritic cells but also the production of MHC class II antigen in dendritic cells, suggesting maturation of these cells. Activation of innate immunity was observed at day 1, peaked at days 3 to 5 after I/R injury, and thereafter gradually decreased.
  
  
  CONCLUSIONS
  I/R injury rapidly activates the innate immune response.
authors.affiliation: Cell Death Research Center, Department of Internal Medicine, The Catholic University of Korea, Seoul, Korea.
authors.forename: Byung Soo
authors.initials: BS
authors.lastname: Kim
authors.forename: Sun Woo
authors.initials: SW
authors.lastname: Lim
authors.forename: Can
authors.initials: C
authors.lastname: Li
authors.forename: Jung Shim
authors.initials: JS
authors.lastname: Kim
authors.forename: Bo Kyung
authors.initials: BK
authors.lastname: Sun
authors.forename: Kyung Ohk
authors.initials: KO
authors.lastname: Ahn
authors.forename: Sang Woo
authors.initials: SW
authors.lastname: Han
authors.forename: Jin
authors.initials: J
authors.lastname: Kim
authors.forename: Chul Woo
authors.initials: CW
authors.lastname: Yang
mesh_terms: D000818:Animals; D000917:Antibody Formation; D003713:Dendritic Cells / Q000378:metabolism / Q000473:pathology; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis / Q000378:metabolism; D007113:Immunity, Innate; D007668:Kidney / Q000276:immunology* / Q000473:pathology; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D015427:Reperfusion Injury / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors
chemical_list: D018840:HSP70 Heat-Shock Proteins; D000949:Histocompatibility Antigens Class II; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; C495343:Tlr2 protein, rat; C495347:Tlr4 protein, rat; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors