title: Influence of TH1/TH2 switched immune response on renal ischemia-reperfusion injury.
abstract: OBJECTIVE
  Recent evidence shows a critical role of the CD4+ T cell with the Th1/Th2 paradigm as a possible effector mechanism in ischemia and reperfusion injury. We hypothesize that a polarized Th1 activation response may negatively influence the renal IRI through its relationship with chemokine production (MCP-1) and with a protective tissue response (HO-1).
  
  
  METHODS
  We subjected mice to renal ischemia for 45 min using IL-4 and IL-12 knockout C57BL/6. We then measured serum urea levels, performed histomorphometric analysis for tubular necrosis and regeneration, and evaluated the mRNA expression of HO-1, t-bet, Gata-3 and MCP-1 by real-time PCR at 24, 48 and 120 h after surgery.
  
  
  CONCLUSIONS
  The IL-4 knockout mice had a statistically significant rise in serum urea levels post IRI compared with control animals. The IL-12-deficient mice were not affected. The IL-4-deficient mice had a statistically significant increase in tubular injury and impairment in cell regeneration. The IRI in IL-4-deficient mice was accompanied by higher levels of HO-1, t-bet and later up-regulation of MCP-1. These findings suggest that the deleterious effects of the Th1 cell involve increased production of chemokines such as MCP-1.
authors.affiliation: Laboratório de Imunologia Clínica e Experimental, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil.
authors.forename: Vilmar Paiva
authors.initials: VP
authors.lastname: Marques
authors.forename: Giselle Martins
authors.initials: GM
authors.lastname: Gonçalves
authors.forename: Carla Quarin
authors.initials: CQ
authors.lastname: Feitoza
authors.forename: Marcos Antonio
authors.initials: MA
authors.lastname: Cenedeze
authors.forename: Ana Paula
authors.initials: AP
authors.lastname: Fernandes Bertocchi
authors.forename: Marcio Jose
authors.initials: MJ
authors.lastname: Damião
authors.forename: Helady Sanders
authors.initials: HS
authors.lastname: Pinheiro
authors.forename: Vicente Paula
authors.initials: VP
authors.lastname: Antunes Teixeira
authors.forename: Marlene Antônia
authors.initials: MA
authors.lastname: dos Reis
authors.forename: Alvaro
authors.initials: A
authors.lastname: Pacheco-Silva
authors.forename: Niels Olsen
authors.initials: NO
authors.lastname: Saraiva Câmara
mesh_terms: D058186:Acute Kidney Injury / Q000276:immunology*; D000818:Animals; D018932:Chemokine CCL2 / Q000235:genetics; D051547:Heme Oxygenase-1 / Q000235:genetics; D018664:Interleukin-12 / Q000172:deficiency; D015847:Interleukin-4 / Q000172:deficiency; D007668:Kidney / Q000276:immunology*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D012038:Regeneration / Q000276:immunology; D015427:Reperfusion Injury / Q000276:immunology*; D020825:T-Box Domain Proteins; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*; D014157:Transcription Factors / Q000235:genetics; D000098815:T-bet Transcription Factor
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D008565:Membrane Proteins; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D014157:Transcription Factors; D018664:Interleukin-12; D015847:Interleukin-4; D051547:Heme Oxygenase-1; C496542:Hmox1 protein, mouse