Early exposure to germs modifies kidney damage and inflammation after experimental ischemia-reperfusion injury

Hye Ryoun Jang, Maria Teresa Gandolfo, Gang Jee Ko, Shailesh Satpute, Lorraine Racusen, Hamid Rabb

Research output: Contribution to journalArticlepeer-review

77 Citations (Scopus)


Kidney ischemia-reperfusion injury (IRI) is, in part, mediated by immune and inflammatory factors. Since microbial stimuli are known to alter immune and inflammatory responses, we hypothesized that differences in perinatal microbial status would modify renal injury following IRI. We performed bilateral renal IRI on 6-wk-old germ-free and control mice and studied the effects on kidney lymphocyte trafficking, cytokines, function, and structure. Compared with control mice, normal kidneys of germ-free mice exhibited more NKT cells and lower IL-4 levels. Postischemia, more CD8 T cells trafficked into postischemic kidneys of germ-free mice compared with control mice. Renal structural injury and functional decline following IRI were more severe in germ-free mice compared with control mice. When germ-free mice were conventionalized with the addition of bacteria to their diet, the extent of renal injury after IRI became equivalent to age-matched control mice, with similar numbers and phenotypes of T cells and NKT cells, as well as cytokine expression in both normal kidneys and postischemic kidneys of conventionalized germ-free mice and age-matched control mice. Thus microbial stimuli influence the phenotype of renal lymphocytes and the expression of cytokines of normal kidneys and also modulate the outcome of IRI.

Original languageEnglish
Pages (from-to)F1457-F1465
JournalAmerican Journal of Physiology - Renal Physiology
Issue number5
Publication statusPublished - 2009 Nov
Externally publishedYes


  • Germ-free status
  • Immune modulation

ASJC Scopus subject areas

  • Physiology
  • Urology


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