Ischemia-Reperfusion Injury Enhances Dendritic Cell Infiltration and TLR2 Expression in Rat Kidneys.
- Author:
Sang Woo HAN
1
;
Byung Soo KIM
;
Sun Woo LIM
;
Bum Soon CHOI
;
Chul Woo YANG
;
Yong Soo KIM
;
Suk Young KIM
;
Euy Jin CHOI
;
Yoon Sik CHANG
;
Byung Kee BANG
Author Information
1. Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea. yangch@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Ischemia/reperfusion injury;
Toll- like receptor;
Dendritic cell;
MHC class II antigen
- MeSH:
Animals;
Antibodies, Monoclonal;
Constriction;
Dendritic Cells*;
Histocompatibility Antigens Class II;
Immunity, Innate;
Immunohistochemistry;
In Situ Hybridization;
Kidney*;
Rats*;
Rats, Sprague-Dawley;
Renal Artery;
Reperfusion Injury*;
RNA, Messenger;
Toll-Like Receptors
- From:Korean Journal of Nephrology
2005;24(5):718-728
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: It is well known that ischemia/reperfusion (I/R) injury enhances immunogenicity. But, its influence on innate immunity is still undetermined. This study was performed to evaluate whether I/R injury activates innate immunity in rat kidneys. METHODS: Sprague-Dawley rats were used. Ischemic injury was induced by clamping both renal arteries for 45 minutes. Sham operation was performed in a similar manner, except clamping the renal vessels. Rats were sacrificed on day 1, 3, 5, and 7 after I/R injury. Activation of innate immunity was evaluated in terms of toll-like receptor (TLR), dendritic cells and MHC class II antigen. TLR2 mRNA expression was detected by RT-PCR, and in situ hybridization. Dendritic cells and MHC class II antigens were detected with OX62 and OX6 monoclonal antibodies by immunohistochemistry. RESULTS: TLR2 mRNA was significantly increased in on day 3 and 5 after I/R injury (1 d: 120+/-2%, 3 d: 137+/-5%, 5 d: 173+/-5% 7 d: 120+/-8% vs. 100+/-11%, p<0.05 vs. sham), and in situ hybridization signal was observed on proximal, distal tubules, and interstitial cells. Compared to the sham-operated rat kidneys, number of dendritic cells significantly increased from day 1 to day 7 after I/R injury (1 d: 22.9+/-2.4, 3 d: 25.8+/-4.9, 5 d: 26.5+/-2.3, 7 d: 24.3+/-1.6 vs. 13.3+/-1.1, p<0.05 vs. sham) with peak value at day 5. Increased expression of MHC class II antigen was observed in the proximal tubules and interstitial cells in I/R injured rat kidney and there was maximal MHC class II protein level on day 3 after I/R injury. CONCLUSION: Ischemia-reperfusion injury itself can activate innate immunity on early period after injury.
