title: High renal ischemia temperature increases neutrophil chemoattractant production and tissue injury during reperfusion without an identifiable role for CD4 T cells in the injury.
abstract: Various leukocyte populations, including neutrophils and CD4 T cells, have been implicated as mediators of acute renal ischemic injury. The influence of ischemic temperature on molecular and cellular mechanisms mediating this injury was tested in a mouse model. Wild-type C57BL/6, B6.CD4(-/-), B6.CD8(-/-), and B6.RAG-1(-/-) mice subjected to bilateral renal pedicle occlusion for 30 min at a higher (37 degrees C) but not a lower (32 degrees C) ischemic maintenance temperature had clear evidence of renal dysfunction and histopathology. Ischemia imposed at the higher temperature also increased CXCL1/KC and CXCL2/MIP-2 levels and neutrophils, but not T cells or macrophages, infiltrating into the ischemic kidneys. Depletion of neutrophils but not T cells attenuated the acute ischemic injury. These results indicate the influence of ischemic temperature and time on the production of neutrophil chemoattractants and subsequent neutrophil infiltration to mediate acute ischemic injury but fail to identify a role for adaptive immune components in this injury.
authors: Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA.
authors: Nobuyuki
authors: N
authors: Fukuzawa
authors: Austin D
authors: AD
authors: Schenk
authors: Marianne
authors: M
authors: Petro
authors: Katsuya
authors: K
authors: Nonomura
authors: William M
authors: WM
authors: Baldwin
authors: Robert L
authors: RL
authors: Fairchild
mesh_terms: D000818:Animals; D017209:Apoptosis; D001831:Body Temperature / Q000502:physiology*; D015704:CD4 Antigens / Q000235:genetics; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000276:immunology; D016827:CD8 Antigens / Q000235:genetics; D018414:CD8-Positive T-Lymphocytes / Q000166:cytology; D002199:Capillary Permeability; D002452:Cell Count; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D054360:Chemokine CXCL1 / Q000235:genetics / Q000378:metabolism; D054426:Chemokine CXCL2 / Q000235:genetics / Q000378:metabolism; D002630:Chemotactic Factors / Q000235:genetics / Q000378:metabolism*; D003404:Creatinine / Q000097:blood; D016207:Cytokines / Q000235:genetics; D015870:Gene Expression / Q000235:genetics; D018398:Homeodomain Proteins / Q000235:genetics; D007668:Kidney / Q000098:blood supply / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D008212:Lymphocyte Depletion; D008264:Macrophages / Q000166:cytology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009504:Neutrophils / Q000166:cytology / Q000276:immunology*; D009195:Peroxidase / Q000378:metabolism; D015427:Reperfusion Injury / Q000276:immunology* / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology
chemical_list: D015704:CD4 Antigens; D016827:CD8 Antigens; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D054360:Chemokine CXCL1; D054426:Chemokine CXCL2; D002630:Chemotactic Factors; C475895:Cxcl1 protein, mouse; C404915:Cxcl2 protein, mouse; D016207:Cytokines; D018398:Homeodomain Proteins; C064658:RAG-1 protein; D003404:Creatinine; D009195:Peroxidase