4.5 Article

Depletion of Macrophages and Dendritic Cells in Ischemic Acute Kidney Injury

期刊

AMERICAN JOURNAL OF NEPHROLOGY
卷 35, 期 2, 页码 181-190

出版社

KARGER
DOI: 10.1159/000335582

关键词

Macrophages; Dendritic cells; Ischemia; Acute kidney injury

资金

  1. American Heart Association (AHA)
  2. [RO1DK056851]
  3. [RO1DK056851S1]
  4. [KO8DK069512]
  5. [R01HL095363]
  6. [AI06877]
  7. [AI066121]
  8. [F32DK079547-01]
  9. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL095363] Funding Source: NIH RePORTER
  10. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI066121] Funding Source: NIH RePORTER
  11. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [K08DK069512, F32DK079547, R01DK056851] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Background: Inflammation is thought to play a role in ischemic acute kidney injury (AKI). We have demonstrated that macrophage and dendritic cell depletion, using liposome-encapsulated clodronate (LEC), is protective against ischemic AKI. Methods: To determine whether macrophages or dendritic cells or both play a role in ischemic AKI, we performed ischemic AKI in CD11b-DTR mice that have a diphtheria toxin (DT)-induced depletion of CD11b cells (macrophages) and CD11c-DTR mice that have a DT-induced depletion of CD11c cells (dendritic cells). Results: While LEC-treated animals had a significant functional protection from AKI, CD11b-DTR and CD11c-DTR mice were not protected against AKI despite a similar degree of renal macrophage and dendritic cell depletion. Proinflammatory cytokines are known to play a role in ischemic AKI. To determine the possible reasons for the lack of protection in CD11b-DTR and CD11c-DTR mice compared to LEC-treated mice, 32 cytokines/chemokines were measured in these mice. Of the cytokines/chemokines measured, IL-6, MCP-1, GMCSF, IL-1 beta and CXCL1 (also known as IL-8 in humans or KC in mice) showed significant differences in the LEE-treated, CD11b-DTR and CD11c-DTR mice. MCP-1 and CXCL1 (known mediators of AKI), and also GMCSF and IL-1 beta were increased in AKI and decreased in LEC-treated AKI but not AKI in CD11b-DTR or CD11c-DTR mice. Conclusions: These findings suggest that LEC-mediated protection from AKI is not simply mediated by depletion of renal macrophage or dendritic cell subpopulations. Protection against AKI in LEC-treated compared to CD11b-DTR or CD11c-DTR mice may be partially explained by differences in proinflammatory cytokine profiles. Copyright (C) 2012 S. Karger AG, Basel

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