Depletion of kidney CD11c+ F4/80+ cells impairs the recovery process in ischaemia/reperfusion-induced acute kidney injury

Myung-Gyu Kim, Chang Su Boo, Yoon Sook Ko, Hee Young Lee, Won Yong Cho, Hyoung Kyu Kim, Sang Kyung Jo

Research output: Contribution to journalArticle

57 Citations (Scopus)

Abstract

Background. Recent studies provided evidence of the potential role of CD11c+ F4/80+ dendritic subset in mediating injury and repair. The purpose of this study was to examine the role of kidney CD11c + F4/80+ dendritic subset in the recovery phase of ischaemia/reperfusion injury (IRI).Methods. Following ischaemia/reperfusion (I/R), liposome clodronate or phosphate buffered saline (PBS) was administered, and on day 7 biochemical and histologic kidney damage was assessed. Activation and depletion of CD11c+ F4/80+ dendritic subset were confirmed by flow cytometry. Isolation of kidney CD11c+ cells on days 1 and 7 with in vitro culture for measuring cytokines was performed to define functional characteristics of these cells, and adoptive transfer of CD11c + cells was also done.Results. Following kidney IRI, the percentage of CD11c+ F4/80+ kidney dendritic cell subset that co-expresses maturation marker increased. Liposome clodronate injection after I/R resulted in preferential depletion of CD11c+ F4/80+ kidney dendritic subset, and depletion of these cells was associated with persistent kidney injury, more apoptosis, inflammation and impaired tubular cell proliferation. CD11c+ F4/80+ cell depletion was also associated with higher tissue levels of pro-inflammatory cytokines and lower level of IL-10, indicating the persistence of inflammatory milieu. Isolated kidney CD11c+ cells on day 7 showed different phenotype with increased production of IL-10 compared with those on day 1. Adoptive transfer of CD11c+ cells partially reversed impaired tissue recovery.Conclusion. Our results suggest that kidney CD11c+ F4/80+ dendritic subset might contribute to the recovery process by dynamic phenotypic change from pro-inflammatory to anti-inflammatory with modulation of immune response.

Original languageEnglish
Pages (from-to)2908-2921
Number of pages14
JournalNephrology Dialysis Transplantation
Volume25
Issue number9
DOIs
Publication statusPublished - 2010 Sep 1

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Acute Kidney Injury
Reperfusion
Ischemia
Kidney
Clodronic Acid
Adoptive Transfer
Reperfusion Injury
Liposomes
Interleukin-10
Cytokines
Wounds and Injuries
Dendritic Cells
Flow Cytometry
Anti-Inflammatory Agents
Phosphates
Cell Proliferation
Apoptosis
Inflammation
Phenotype
Injections

Keywords

  • acute kidney injury
  • dendritic subset
  • liposome clodronate
  • recovery

ASJC Scopus subject areas

  • Nephrology
  • Transplantation

Cite this

Depletion of kidney CD11c+ F4/80+ cells impairs the recovery process in ischaemia/reperfusion-induced acute kidney injury. / Kim, Myung-Gyu; Su Boo, Chang; Sook Ko, Yoon; Young Lee, Hee; Cho, Won Yong; Kyu Kim, Hyoung; Jo, Sang Kyung.

In: Nephrology Dialysis Transplantation, Vol. 25, No. 9, 01.09.2010, p. 2908-2921.

Research output: Contribution to journalArticle

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abstract = "Background. Recent studies provided evidence of the potential role of CD11c+ F4/80+ dendritic subset in mediating injury and repair. The purpose of this study was to examine the role of kidney CD11c + F4/80+ dendritic subset in the recovery phase of ischaemia/reperfusion injury (IRI).Methods. Following ischaemia/reperfusion (I/R), liposome clodronate or phosphate buffered saline (PBS) was administered, and on day 7 biochemical and histologic kidney damage was assessed. Activation and depletion of CD11c+ F4/80+ dendritic subset were confirmed by flow cytometry. Isolation of kidney CD11c+ cells on days 1 and 7 with in vitro culture for measuring cytokines was performed to define functional characteristics of these cells, and adoptive transfer of CD11c + cells was also done.Results. Following kidney IRI, the percentage of CD11c+ F4/80+ kidney dendritic cell subset that co-expresses maturation marker increased. Liposome clodronate injection after I/R resulted in preferential depletion of CD11c+ F4/80+ kidney dendritic subset, and depletion of these cells was associated with persistent kidney injury, more apoptosis, inflammation and impaired tubular cell proliferation. CD11c+ F4/80+ cell depletion was also associated with higher tissue levels of pro-inflammatory cytokines and lower level of IL-10, indicating the persistence of inflammatory milieu. Isolated kidney CD11c+ cells on day 7 showed different phenotype with increased production of IL-10 compared with those on day 1. Adoptive transfer of CD11c+ cells partially reversed impaired tissue recovery.Conclusion. Our results suggest that kidney CD11c+ F4/80+ dendritic subset might contribute to the recovery process by dynamic phenotypic change from pro-inflammatory to anti-inflammatory with modulation of immune response.",
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AU - Sook Ko, Yoon

AU - Young Lee, Hee

AU - Cho, Won Yong

AU - Kyu Kim, Hyoung

AU - Jo, Sang Kyung

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N2 - Background. Recent studies provided evidence of the potential role of CD11c+ F4/80+ dendritic subset in mediating injury and repair. The purpose of this study was to examine the role of kidney CD11c + F4/80+ dendritic subset in the recovery phase of ischaemia/reperfusion injury (IRI).Methods. Following ischaemia/reperfusion (I/R), liposome clodronate or phosphate buffered saline (PBS) was administered, and on day 7 biochemical and histologic kidney damage was assessed. Activation and depletion of CD11c+ F4/80+ dendritic subset were confirmed by flow cytometry. Isolation of kidney CD11c+ cells on days 1 and 7 with in vitro culture for measuring cytokines was performed to define functional characteristics of these cells, and adoptive transfer of CD11c + cells was also done.Results. Following kidney IRI, the percentage of CD11c+ F4/80+ kidney dendritic cell subset that co-expresses maturation marker increased. Liposome clodronate injection after I/R resulted in preferential depletion of CD11c+ F4/80+ kidney dendritic subset, and depletion of these cells was associated with persistent kidney injury, more apoptosis, inflammation and impaired tubular cell proliferation. CD11c+ F4/80+ cell depletion was also associated with higher tissue levels of pro-inflammatory cytokines and lower level of IL-10, indicating the persistence of inflammatory milieu. Isolated kidney CD11c+ cells on day 7 showed different phenotype with increased production of IL-10 compared with those on day 1. Adoptive transfer of CD11c+ cells partially reversed impaired tissue recovery.Conclusion. Our results suggest that kidney CD11c+ F4/80+ dendritic subset might contribute to the recovery process by dynamic phenotypic change from pro-inflammatory to anti-inflammatory with modulation of immune response.

AB - Background. Recent studies provided evidence of the potential role of CD11c+ F4/80+ dendritic subset in mediating injury and repair. The purpose of this study was to examine the role of kidney CD11c + F4/80+ dendritic subset in the recovery phase of ischaemia/reperfusion injury (IRI).Methods. Following ischaemia/reperfusion (I/R), liposome clodronate or phosphate buffered saline (PBS) was administered, and on day 7 biochemical and histologic kidney damage was assessed. Activation and depletion of CD11c+ F4/80+ dendritic subset were confirmed by flow cytometry. Isolation of kidney CD11c+ cells on days 1 and 7 with in vitro culture for measuring cytokines was performed to define functional characteristics of these cells, and adoptive transfer of CD11c + cells was also done.Results. Following kidney IRI, the percentage of CD11c+ F4/80+ kidney dendritic cell subset that co-expresses maturation marker increased. Liposome clodronate injection after I/R resulted in preferential depletion of CD11c+ F4/80+ kidney dendritic subset, and depletion of these cells was associated with persistent kidney injury, more apoptosis, inflammation and impaired tubular cell proliferation. CD11c+ F4/80+ cell depletion was also associated with higher tissue levels of pro-inflammatory cytokines and lower level of IL-10, indicating the persistence of inflammatory milieu. Isolated kidney CD11c+ cells on day 7 showed different phenotype with increased production of IL-10 compared with those on day 1. Adoptive transfer of CD11c+ cells partially reversed impaired tissue recovery.Conclusion. Our results suggest that kidney CD11c+ F4/80+ dendritic subset might contribute to the recovery process by dynamic phenotypic change from pro-inflammatory to anti-inflammatory with modulation of immune response.

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