PMID- 17311071
OWN - NLM
STAT- MEDLINE
DCOM- 20070629
LR  - 20181201
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 71
IP  - 7
DP  - 2007 Apr
TI  - Resident dendritic cells are the predominant TNF-secreting cell in early renal 
      ischemia-reperfusion injury.
PG  - 619-28
AB  - Renal ischemia-reperfusion injury (IRI) rapidly induces production of 
      inflammatory mediators including, and in particular, tumor necrosis factor (TNF). 
      Possible sources include resident parenchymal and bone marrow-derived cells as 
      well as recruited leukocytes. Cell suspensions from kidneys subjected to IRI were 
      examined by cell separation followed by in vitro culture and enzyme-linked 
      immunosorbent assay (ELISA), immunoperoxidase and immunofluorescence microscopy, 
      and multicolor flow cytometry to determine the contribution of dendritic cells 
      (DCs) to early production of TNF and other inflammatory mediators. Secretion of 
      TNF, interleukin (IL-6), monocyte chemoattractant protein-1 (MCP-1), and 
      regulated on activation normal T cell expressed and secreted (RANTES) was 
      increased in cell suspensions from IRI compared with control kidneys and was 
      higher in DC-enriched preparations. Immunostaining identified TNF(+ve) cells that 
      coexpressed the DC marker CD11c. Flow cytometry of bone marrow-derived 
      (CD45(+ve)) cell populations at 24 h post-IRI demonstrated that 
      F4/80(+ve)/CD11c(+ve) DCs remained proportionately stable and exhibit higher 
      levels of DC maturation markers, whereas the proportion of F4/80(-ve) DCs, 
      monocytes, neutrophils, and T cells increased. Intracellular staining for TNF 
      confirmed that F4/80(+ve) DCs were the predominant TNF(+ve) cell and expressed 
      higher levels than other TNF(+ve) cells. In vivo depletion of DCs from the kidney 
      substantially attenuated TNF secretion by total and CD45(+ve) cells following 
      IRI. The results uncover a role for resident F4/80(+ve) DCs as the predominant 
      secretors of TNF within 24 h of IRI.
FAU - Dong, X
AU  - Dong X
AD  - Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic 
      College of Medicine, Rochester, Minnesota, USA.
FAU - Swaminathan, S
AU  - Swaminathan S
FAU - Bachman, L A
AU  - Bachman LA
FAU - Croatt, A J
AU  - Croatt AJ
FAU - Nath, K A
AU  - Nath KA
FAU - Griffin, M D
AU  - Griffin MD
LA  - eng
GR  - D47060/PHS HHS/United States
GR  - DK68545/DK/NIDDK NIH HHS/United States
GR  - T32DK07013/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20070221
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (CD11 Antigens)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
CIN - Kidney Int. 2007 Apr;71(7):604-5. PMID: 17387309
MH  - Animals
MH  - CD11 Antigens/biosynthesis
MH  - Dendritic Cells/*metabolism
MH  - Kidney/*blood supply
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Reperfusion Injury/*immunology
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 2007/02/22 09:00
MHDA- 2007/06/30 09:00
CRDT- 2007/02/22 09:00
PHST- 2007/02/22 09:00 [pubmed]
PHST- 2007/06/30 09:00 [medline]
PHST- 2007/02/22 09:00 [entrez]
AID - S0085-2538(15)52440-X [pii]
AID - 10.1038/sj.ki.5002132 [doi]
PST - ppublish
SO  - Kidney Int. 2007 Apr;71(7):619-28. doi: 10.1038/sj.ki.5002132. Epub 2007 Feb 21.