Fate of Neutrophils during the Recovery Phase of Ischemia/Reperfusion Induced Acute Kidney Injury.
10.3346/jkms.2017.32.10.1616
- Author:
Wonyong CHO
1
;
Jie Young SONG
;
Se Won OH
;
Myung Gyu KIM
;
Yoon Sook KO
;
Hee Yong LEE
;
Sang Kyung JO
Author Information
1. Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea. sang-kyung@korea.ac.kr
- Publication Type:Original Article
- Keywords:
Ischemia/Reperfusion;
Neutrophil;
Apoptosis;
Reverse Transendothelial Migration;
Recovery
- MeSH:
Acute Kidney Injury*;
Animals;
Apoptosis;
Bone Marrow;
Chimera;
Cytokines;
Fibrosis;
Inflammation;
Intercellular Adhesion Molecule-1;
Kidney;
Mice;
Neutrophils*;
Phenotype;
Transendothelial and Transepithelial Migration;
Uromodulin
- From:Journal of Korean Medical Science
2017;32(10):1616-1625
- CountryRepublic of Korea
- Language:English
-
Abstract:
Effective clearance of inflammatory cells is required for resolution of inflammation. Here, we show in vivo evidence that apoptosis and reverse transendothelial migration (rTEM) are important mechanisms in eliminating neutrophils and facilitating recovery following ischemia/reperfusion injury (IRI) of the kidney. The clearance of neutrophils was delayed in the Bax knockout (KO)BM → wild-type (WT) chimera in which bone marrow derived cells are partially resistant to apoptosis, compared to WTBM → WT mice. These mice also showed delayed functional, histological recovery, increased tissue cytokines, and accelerated fibrosis. The circulating intercellular adhesion molecule-1 (ICAM-1)+ Gr-1+ neutrophils displaying rTEM phenotype increased during the recovery phase and blockade of junctional adhesion molecule-C (JAM-C), a negative regulator of rTEM, resulted in an increase in circulating ICAM-1+ neutrophils, faster resolution of inflammation and recovery. The presence of Tamm-Horsfall protein (THP) in circulating ICAM-1+ neutrophils could suggest that they are derived from injured kidneys. In conclusion, we suggest that apoptosis and rTEM are critically involved in the clearance mechanisms of neutrophils during the recovery phase of IRI.
