| Depletion of kidney CD11c+ F4/80+ cells impairs the recovery process in ischaemia/reperfusion-induced acute kidney injury. | |
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MedLine Citation:
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PMID: 20388633 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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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Authors:
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Myung-Gyu Kim; Chang Su Boo; Yoon Sook Ko; Hee Young Lee; Won Yong Cho; Hyoung Kyu Kim; Sang-Kyung Jo |
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Publication Detail:
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Type: Journal Article Date: 2010-04-12 |
Journal Detail:
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Title: Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association Volume: 25 ISSN: 1460-2385 ISO Abbreviation: Nephrol. Dial. Transplant. Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-08-25 Completed Date: 2010-12-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8706402 Medline TA: Nephrol Dial Transplant Country: England |
Other Details:
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Languages: eng Pagination: 2908-21 Citation Subset: IM |
Affiliation:
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Division of Nephrology, Department of Internal Medicine, Korea University Anam Hospital, Korea University College of Medicine, Seoul, Korea. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Kidney Injury
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etiology,
metabolism,
prevention & control* Animals Antigens, CD11c / metabolism* Antigens, CD80 / metabolism* Antigens, CD86 / metabolism Apoptosis / drug effects Blotting, Western Bone Density Conservation Agents / pharmacology Cell Proliferation / drug effects Clodronic Acid / pharmacology Dendritic Cells / cytology, drug effects, metabolism* Flow Cytometry Inflammation Mediators / metabolism Liposomes Male Mice Mice, Inbred C57BL Reperfusion Injury / complications, metabolism, prevention & control* Signal Transduction |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD11c; 0/Antigens, CD80; 0/Antigens, CD86; 0/Bone Density Conservation Agents; 0/Inflammation Mediators; 0/Liposomes; 10596-23-3/Clodronic Acid |
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