Ischemia-reperfusion injury activates innate immunity in rat kidneys
BS Kim, SW Lim, C Li, JS Kim, BK Sun, KO Ahn… - …, 2005 - journals.lww.com
BS Kim, SW Lim, C Li, JS Kim, BK Sun, KO Ahn, SW Han, J Kim, CW Yang
Transplantation, 2005•journals.lww.comBackground. There is growing evidence of a role of the immune system in the
pathophysiology of ischemia-reperfusion (I/R) injury, but the influence of I/R injury on innate
immunity is still undetermined. Methods. Sprague-Dawley rats were used. I/R injury was
induced by clamping both renal arteries for 45 min, and the rats were killed 1, 3, 5, and 7
days later. Activation of innate immunity was evaluated in terms of the expression of toll-like
receptor (TLR) 2 or TLR4 mRNAs and protein, by the level of the TLR ligand (heat shock …
pathophysiology of ischemia-reperfusion (I/R) injury, but the influence of I/R injury on innate
immunity is still undetermined. Methods. Sprague-Dawley rats were used. I/R injury was
induced by clamping both renal arteries for 45 min, and the rats were killed 1, 3, 5, and 7
days later. Activation of innate immunity was evaluated in terms of the expression of toll-like
receptor (TLR) 2 or TLR4 mRNAs and protein, by the level of the TLR ligand (heat shock …
Abstract
Background.
There is growing evidence of a role of the immune system in the pathophysiology of ischemia-reperfusion (I/R) injury, but the influence of I/R injury on innate immunity is still undetermined.
Methods.
Sprague-Dawley rats were used. I/R injury was induced by clamping both renal arteries for 45 min, and the rats were killed 1, 3, 5, and 7 days later. Activation of innate immunity was evaluated in terms of the expression of toll-like receptor (TLR) 2 or TLR4 mRNAs and protein, by the level of the TLR ligand (heat shock protein [HSP] 70), and maturation of dendritic cells by double-label immunohistochemistry of dendritic cells for major histocompatibility complex (MHC) class II antigen.
Results.
I/R injury increased TLR2 and TLR4 mRNA and protein expression, and they were mainly observed on renal tubular cells. I/R injury also produced endogenous TLR ligand (HSP70) on renal tubular cells. I/R injury increased not only the numbers of dendritic cells but also the production of MHC class II antigen in dendritic cells, suggesting maturation of these cells. Activation of innate immunity was observed at day 1, peaked at days 3 to 5 after I/R injury, and thereafter gradually decreased.
Conclusions.
I/R injury rapidly activates the innate immune response.
Ischemia/reperfusion (I/R) injury is unavoidable in renal transplantation. It may increase the immunogenicity of the organ by increasing the production of major histocompatibility complex (MHC) class II antigens, which is closely associated with increased acute rejection episodes. In addition, I/R injury in the early transplant period has been associated with late allograft failure (1–4).
Lippincott Williams & Wilkins