High renal ischemia temperature increases neutrophil chemoattractant production and tissue injury during reperfusion without an identifiable role for CD4 T cells in the injury

Nobuyuki Fukuzawa, Austin D. Schenk, Marianne Petro, Katsuya Nonomura, William M. Baldwin, Robert L. Fairchild

Research output: Contribution to journalArticlepeer-review

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 °C) but not a lower (32 °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.

Original languageEnglish (US)
Pages (from-to)62-71
Number of pages10
JournalTransplant Immunology
Volume22
Issue number1-2
DOIs
StatePublished - Jan 2009
Externally publishedYes

Keywords

  • Acute ischemic injury
  • CD4 and CD8 T cells
  • Chemokines
  • Kidney
  • Mouse model
  • Neutrophil

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Transplantation

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