Ischemia-Reperfusion Injury Enhances Dendritic Cell Infiltration and TLR2 Expression in Rat Kidneys / 대한신장학회잡지

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.