title: Detrimental functions of IL-17A in renal ischemia-reperfusion injury in mice.
abstract: BACKGROUND
  Renal ischemia-reperfusion (I/R) injury, as a common and clinically important problem, starts with direct damage caused by chemokines and inflammatory cytokines, which is aggravated by specific and nonspecific immune reactions. Recently, IL-17A has been considered to be in a uniquely powerful position between adaptive and innate immunity. The present study investigated the role of IL-17A in renal I/R injury in mice.
  
  
  METHODS
  We measured the time-course of changes in plasma and renal IL-17A levels using a murine model of renal I/R injury. Then, the protective effect of monoclonal anti-IL-17A antibody, given intravenously at 30 min before or after renal I/R operation, on renal I/R injury was investigated. In addition, the levels of plasma and renal pro- and anti-inflammatory cytokines and chemokines were assessed.
  
  
  RESULTS
  IL-17A was significantly increased in plasma and kidneys after renal I/R injury in mice. Furthermore, intravenous administration of neutralizing monoclonal anti-IL-17A antibody attenuated renal I/R injury by evaluating renal function and histopathology. In addition, administration of anti-IL-17A antibody substantially reduced the plasma and renal levels of many pro-inflammatory mediators (TNF-α, IL-6, high-mobility group box 1 (HMGB1), IL-1β, IL-17A, macrophage inflammatory protein-1α (MIP-1α), and monocyte chemoattractant protein-1 (MCP-1), as well as increased the plasma and renal levels of anti-inflammatory cytokines IL-10 and transforming growth factor β (TGF-β).
  
  
  CONCLUSIONS
  The above data suggest that IL-17A has a detrimental effect on renal I/R injury via facilitating the production of pro-inflammatory cytokines and chemokines as well as hampering the production of anti-inflammatory cytokines.
authors.affiliation: Department of Urology, Tangdu Hospital of the Fourth Military Medical University, Xi'an, Shaanxi Province, PR China.
authors.forename: Li
authors.initials: L
authors.lastname: Xue
authors.forename: Keliang
authors.initials: K
authors.lastname: Xie
authors.forename: Xiujuan
authors.initials: X
authors.lastname: Han
authors.forename: Zengyue
authors.initials: Z
authors.lastname: Yang
authors.forename: Jianxin
authors.initials: J
authors.lastname: Qiu
authors.forename: Zhiguang
authors.initials: Z
authors.lastname: Zhao
authors.forename: Tingyi
authors.initials: T
authors.lastname: Bao
mesh_terms: D056704:Adaptive Immunity / Q000502:physiology*; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D057134:Antibodies, Neutralizing / Q000494:pharmacology; D016207:Cytokines / Q000097:blood; D004195:Disease Models, Animal; D020381:Interleukin-17 / Q000097:blood* / Q000276:immunology*; D007668:Kidney / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D015427:Reperfusion Injury / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D057134:Antibodies, Neutralizing; D016207:Cytokines; D020381:Interleukin-17; D051996:Transcription Factor RelA