title: Aging has small effects on initial ischemic acute kidney injury development despite changing intrarenal immunologic micromilieu in mice.
abstract: Inflammatory process mediated by innate and adaptive immune systems is a major pathogenic mechanism of renal ischemia-reperfusion injury (IRI). There are concerns that organ recipients may be at increased risk of developing IRI after receiving kidneys from elder donors. To reveal the effects of aging on the development of renal IRI, we compared the immunologic micromilieu of normal and postischemic kidneys from mice of three different ages (9 wk, 6 mo, and 12 mo). There was a higher number of total T cells, especially effector memory CD4/CD8 T cells, and regulatory T cells in the normal kidneys of old mice. On day 2 after IRI, the proportion of necrotic tubules and renal functional changes were comparable between groups although old mice had a higher proportion of damaged tubule compared with young mice. More T cells, but less B cells, trafficked into the postischemic kidneys of old mice. The infiltration of NK T cells was similar across the groups. Macrophages and neutrophils were comparable between groups in both normal kidneys and postischemic kidneys. The intrarenal expressions of TNF-α and VEGF were decreased in normal and postischemic kidneys of aged mice. These mixed effects of aging on lymphocytes and cytokines/chemokines were not different between the two groups of old mice. Our study demonstrates that aging alters the intrarenal micromilieu but has small effects on the development of initial renal injury after IRI. Further study investigating aging-dependent differences in the repair process of renal IRI may be required.
authors.affiliation: Nephrology Division, Department of Medicine, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea;
authors.forename: Hye Ryoun
authors.initials: HR
authors.lastname: Jang
authors.affiliation: Nephrology Division, Department of Medicine, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea;
authors.forename: Ji Hyeon
authors.initials: JH
authors.lastname: Park
authors.affiliation: Department of Pathology, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea;
authors.forename: Ghee Young
authors.initials: GY
authors.lastname: Kwon
authors.affiliation: Department of Surgery, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea; and.
authors.forename: Jae Berm
authors.initials: JB
authors.lastname: Park
authors.affiliation: Nephrology Division, Department of Medicine, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea;
authors.forename: Jung Eun
authors.initials: JE
authors.lastname: Lee
authors.affiliation: Nephrology Division, Department of Medicine, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea;
authors.forename: Dae Joong
authors.initials: DJ
authors.lastname: Kim
authors.affiliation: Nephrology Division, Department of Medicine, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea;
authors.forename: Yoon-Goo
authors.initials: YG
authors.lastname: Kim
authors.affiliation: Department of Surgery, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea; and.
authors.forename: Sung Joo
authors.initials: SJ
authors.lastname: Kim
authors.affiliation: Nephrology Division, Department of Medicine, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea;
authors.forename: Ha Young
authors.initials: HY
authors.lastname: Oh
authors.affiliation: Nephrology Division, Department of Medicine, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea; Department of Clinical Pharmacology and Therapeutics, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea wooseong.huh@samsung.com.
authors.forename: Wooseong
authors.initials: W
authors.lastname: Huh
mesh_terms: D058186:Acute Kidney Injury / Q000276:immunology* / Q000473:pathology*; D000375:Aging / Q000473:pathology*; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D015850:Interleukin-6 / Q000096:biosynthesis / Q000235:genetics; D007668:Kidney / Q000276:immunology* / Q000473:pathology*; D007677:Kidney Function Tests; D007684:Kidney Tubules / Q000473:pathology; D017493:Leukocyte Common Antigens / Q000096:biosynthesis; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009336:Necrosis; D009195:Peroxidase / Q000378:metabolism; D015427:Reperfusion Injury / Q000276:immunology / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis / Q000235:genetics
chemical_list: D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; C577686:interleukin-6, mouse; C467480:vascular endothelial growth factor A, mouse; D009195:Peroxidase; D017493:Leukocyte Common Antigens
keywords: aging; inflammation; ischemia-reperfusion injury