Modulation of monocyte-derived dendritic cell differentiation is associated with ischemic acute renal failure.
BACKGROUND
Dendritic cells (DCs) play a central role in both stimulating and suppressing immune responses and are impacted by surgical injury, exercise, and other physiological stressors. This study aims to determine whether renal ischemia/reperfusion (I/R) injury alters the differentiation, maturation, and activation of DCs from peripheral blood monocytes (PBMo).


METHODS
Sprague-Dawley (SD) rats were subjected to I/R injury or sham-operated. Creatinine clearance (CCr) was monitored daily during the 14 days of reperfusion that followed the ischemic insult. At 2 and 14 days of reperfusion, the following properties of PBMo derived-DCs were assessed: the amount of generated DCs, surface markers [CD11c, CD80, CD86, and MHC-II (IA)], and functional status including magnitude of mixed lymphocyte reaction (MLR), production of IL-12 p70 by DCs, and production of IFN-gamma and IL-4 by DC-stimulated T cells.


RESULTS
CCr was greatly reduced in the injured rats 0 to 4 days after ischemia. Two days after I/R injury to kidney, the numbers of DCs differentiated from PBMo, IL-12 production by DCs, expression of MHC-II (IA), and IFN-gamma production by DC-stimulated T cells were significantly increased in the I/R injured group (compared to the sham-operated group). After 14 days of reperfusion, there was no between-group differences in the numbers of DCs derived from PBMo, MLR, expression of CD80, CD86, and MHC-II (IA), and production of IL-12, IFN-gamma, and IL-4.


CONCLUSIONS
The increases seen at 2 days of reperfusion may reflect a preparatory step in the renal I/R injury pathway. The relationship between up-regulation of DC differentiation and ischemic acute renal failure (ARF) remains to be elucidated.
Wu
Chih-Jen
CJ
Graduate Institute of Medical Science, Taipei Medical University, Taipei, Taiwan.
Sheu
Joen-Rong
JR
Chen
Han-Hsiang
HH
Liao
Hui-Fen
HF
Yang
Yuh-Cheng
YC
Yang
Stone
S
Chen
Yu-Jen
YJ
D058186:Acute Kidney Injury / Q000276:immunology* / Q000503:physiopathology*; D000818:Animals; D000943:Antigens, Differentiation / Q000032:analysis; D002454:Cell Differentiation; D003713:Dendritic Cells / Q000276:immunology* / Q000473:pathology; D004195:Disease Models, Animal; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D007371:Interferon-gamma / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D007511:Ischemia / Q000276:immunology* / Q000503:physiopathology*; D009000:Monocytes / Q000276:immunology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation; D015427:Reperfusion Injury / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D000943:Antigens, Differentiation; D000949:Histocompatibility Antigens Class II; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4; D007371:Interferon-gamma