Separated parabiont reveals the fate and lifespan of peripheral-derived immune cells in normal and ischaemia-induced injured kidneys.
Separated parabiont reveals the fate and lifespan of peripheral-derived immune cells in normal and ischaemia-induced injured kidneys.
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分离的共生体揭示了正常和缺血引起的损伤肾脏中外周源性免疫细胞的命运和寿命
DOI:
10.1098/rsob.200340
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发表时间:
2021-06
期刊:
影响因子:
5.8
通讯作者:
Xu G
中科院分区:
文献类型:
--
作者:
Deng X;Zhou C;Liao R;Guo Y;Wang Y;Li G;Wu J;Xu H;Hu Z;Pei G;Liao W;Yao Y;Yang Q;Zeng R;Xu G
Immune cell infiltration plays a key role in acute kidney injury (AKI) to chronic kidney disease (CKD) progression. T lymphocytes, neutrophils, monocytes/macrophages and other immune cells regulate inflammation, tissue remodelling and repair. To determine the kinetics of accumulation of various immune cell populations, we established an animal model combining parabiosis and separation surgery to explore the fate and lifespan of peripheral leucocytes that migrate to the kidney. We found that peripheral T lymphocytes could survive for a long time (more than 14 days), whereas peripheral neutrophils survived for a short time in both healthy and ischaemia-induced damaged kidneys. Nearly half of the peripheral-derived macrophages disappeared after 14 days in normal kidneys, while their existing time in the inflammatory kidneys was prolonged. A fraction of F4/80high macrophages were renewed from the circulating monocyte pool. In addition, we found that after renal ischaemia reperfusion, neutrophils increased significantly in the early phase, and T lymphocytes mainly accumulated in the late stage, whereas macrophages infiltrated throughout AKI-CKD progression and were sustained longer in injured as opposed to normal kidneys. In conclusion, peripheral-derived macrophages, T lymphocytes and neutrophils exhibit different lifespans in the kidney, which may play different roles during AKI-CKD progression.
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DOI:
10.1053/j.ajkd.2012.03.014
发表时间:
2012-09
期刊:
American journal of kidney diseases : the official journal of the National Kidney Foundation
影响因子:
--
作者:
Jones J;Holmen J;De Graauw J;Jovanovich A;Thornton S;Chonchol M
通讯作者:
Chonchol M
影响因子:
30.5
作者:
Goldmann T;Wieghofer P;Jordão MJ;Prutek F;Hagemeyer N;Frenzel K;Amann L;Staszewski O;Kierdorf K;Krueger M;Locatelli G;Hochgerner H;Zeiser R;Epelman S;Geissmann F;Priller J;Rossi FM;Bechmann I;Kerschensteiner M;Linnarsson S;Jung S;Prinz M
通讯作者:
Prinz M
影响因子:
2.9
作者:
Feng Nan;Luo Jianmin;Guo Ximin
通讯作者:
Guo Ximin
影响因子:
19.6
作者:
Dong, Xiangyang;Bachman, Lori A.;Miller, Melinda N.;Nath, Karl A.;Griffin, Matthew D.
通讯作者:
Griffin, Matthew D.
影响因子:
19.6
作者:
Dong, X.;Swaminathan, S.;Griffin, M. D.
通讯作者:
Griffin, M. D.