The investigation of macrophage infiltration in the early phase of ischemic acute renal failure in mice.
10.3904/kjim.2008.23.2.64
- Author:
Soo Jeong YU
1
;
Dong Jin OH
;
Suk Hee YU
Author Information
1. Department of Internal Medicine, Incheon Christian Hospital, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Acute renal failure;
Ischemia;
Inflammation;
Macrophages
- MeSH:
Animals;
Antigens, CD11b;
Blood Urea Nitrogen;
Clodronic Acid;
Creatinine/blood;
Fluorescent Antibody Technique;
Inflammation/*physiopathology;
Ischemia/*complications/pathology/physiopathology;
Kidney Failure, Acute/blood/etiology/*pathology/physiopathology;
Kidney Medulla/*pathology;
*Macrophages;
Male;
Mice;
Mice, Inbred C57BL;
Perfusion;
Time Factors
- From:The Korean Journal of Internal Medicine
2008;23(2):64-71
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/AIMS: Inflammation plays a key role in ischemic acute renal failure (ARF). The present study investigated the infiltration of macrophages in the early phase of ischemic ARF in mice. METHODS: Ischemic ARF was induced by renal clamping for 22 min, while the control mice underwent sham surgery (no clamping). The serum creatinine and blood urea nitrogen (BUN) levels were measured in the control and post-ischemia mice. Immunofluorescence staining was used to measure the number of CD 11b-positive cells in the kidney tissue sections to determine the amount of post-ischemic macrophage infiltration. Lipo-Cl2MBP (clodronate) for macrophages depletion was injected via a tail vein 5 d before ischemia induction and again 2 d before ischemia induction. RESULTS: The study found that the post-ischemia mice had higher levels of serum creatinine and BUN at 16 and 24 h compared to the controls. Immunofluorescence staining showed there were more macrophages in the post-ischemic tissue at 2, 8, 16 and 24 h compared to the control tissue, and that most of these macrophages were located in the outer medulla. The mice treated with clodronate prior to ischemia induction were found to have lower levels of serum creatinine compared to those mice that weren't treated with clodronate. CONCLUSIONS: There was significant infiltration of macrophages from the early phase of ischemic ARF, and this peaked at 16-24 h. Macrophage depletion using clodronate was protective against ischemic ARF.
