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Kidney Week

Abstract: TH-PO086

Aging and Immune Response to the Late Recovery Phase of Ischemic AKI

Session Information

  • AKI: Mechanisms - I
    November 02, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Jeon, Hojin, Samsung Medical Center, Cell and Gene Therapy Institute, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Lee, Kyungho, Samsung Medical Center, Cell and Gene Therapy Institute, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Jeon, Junseok, Samsung Medical Center, Cell and Gene Therapy Institute, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Lee, Jung eun, Samsung Medical Center, Cell and Gene Therapy Institute, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Huh, Wooseong, Samsung Medical Center, Cell and Gene Therapy Institute, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Kim, Yoon-Goo, Samsung Medical Center, Cell and Gene Therapy Institute, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
  • Jang, Hye Ryoun, Samsung Medical Center, Cell and Gene Therapy Institute, Sungkyunkwan University School of Medicine, Seoul, Korea (the Republic of)
Background

Kidney immune cells play important roles in acute kidney injury (AKI) and the repair process. Considering that aging affects immune cell compositions and their function in multiple organs, the effect of aging on kidney and extrarenal immune responses in the recovery phase after ischemic AKI was evaluated.

Methods

C57Bl/6 mice with three different age groups, including 7-week, 6- and 12-month-old, underwent unilateral ischemia-reperfusion injury (UIRI) for 45 min. Mice were followed up until 4 weeks, and kidneys and spleens were collected. Serum creatinine and cystatin-C levels were measured. Kidney and splenic lymphocytes were analyzed by flow cytometry.

Results

Serum creatinine (7-week-old, 0.25±0.05; 6-month-old, 0.41±0.04, P=0.01; 12-month-old, 0.39±0.02mg/dL, P<0.01) and cystatin-C (548.67±30.35; 545.00±30.25, P=0.99; 914.60±96.40ng/ml, P=0.01) levels were higher in older mice at 4 weeks after UIRI, although both were comparable between groups at baseline. NK T cells (6.27±0.47 vs 2.51±0.30%, P<0.01) and Tregs (13.42±1.11 vs 7.87±0.53%, P<0.01) were lower in post-ischemic kidneys of 12-month-old mice than 7-week-old mice, whereas they were comparable in contralateral kidneys (NK T cells, 10.83±1.10 vs 9.56±0.65%, P=0.82; Tregs, 2.13±0.15 vs 2.13± 0.62%, P=0.99). There were no differences in the proportion of CD4 T cells and CD8 T cells among total T cells in both post-ischemic and contralateral kidneys. Activated B cells from older mice were higher in post-ischemic kidneys (10.00±1.06; 16.37±2.01, P=0.04; 19.77±1.74%, P<0.01) as well as in contralateral kidneys (2.78±0.19; 6.52±1.07, P<0.01; 7.81±0.42%, P<0.01). Splenic CD4 T cells (60.13±1.68 vs 91.32±2.35% of total T cells, P<0.01) were higher, and splenic Tregs (8.30±0.33 vs 5.34±1.22% of CD4 T cells, P=0.03) were lower in 12-month-old mice compared to 6-month-old mice. Splenic T cells from older mice had higher expression of CD69 (7.83±0.30; 15.95±2.05, P=0.097; 19.62±3.93% of total T cells, P=0.01).

Conclusion

Aging affects long-term intrarenal and systemic immune responses to ischemic AKI during the recovery phase. Older hosts showed an accelerated proinflammatory and diminished anti-inflammatory responses. Future studies are needed to evaluate senescent immune reaction in ischemic AKI.