Abstract
BackgroundIn the early stage of sepsis, M1 macrophages result in the production of inflammatory mediators and AKI. Heparin-binding protein (HBP) have been shown to play important roles in sepsis-induced AKI. In this study, we investigate the association of HBP with M1 macrophages in sepsis-induced AKI.MethodsMale C57BL6 mice were subjected to cecal ligation and puncture (CLP) or sham surgery. Biochemical and histological renal damage was assessed. Macrophage infiltration was assessed by immunohistochemistry. RT-PCR was used to investigate the expression of heparin-binding protein (HBP), the inducible nitric oxide synthase (iNOS) and arginase 1 (Arg-1) mRNAs. Western blots were performed to assay the tissue levels of HBP, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6).ResultsHigh levels of HBP were obviously detected 24 h after sepsis-induced AKI. Heparin inhibited HBP expression during sepsis-induced AKI. The suppression of HBP expression by heparin injection after the establishment of sepsis-induced AKI resulted in a reduction in renal injury severity accompanied with a significant repression of M1 macrophage activation and expression of TNF-α and IL-6.ConclusionsHBP plays an important role in the initial inflammatory reaction associated with sepsis-induced AKI, presumably by activating M1 macrophages and suppressing TNF-α and IL-6 secretion.
Highlights
Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with increased morbidity and mortality [1]
RT-PCR was used to investigate the expression of heparin-binding protein (HBP), the inducible nitric oxide synthase and arginase 1 (Arg-1) mRNAs
The suppression of Heparin-binding protein (HBP) expression by heparin injection after the establishment of sepsis-induced AKI resulted in a reduction in renal injury severity accompanied with a significant repression of M1 macrophage activation and expression of TNF-α and IL-6
Summary
Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with increased morbidity and mortality [1]. Sepsis-induced AKI is caused by a combination of multiple mechanisms, including inadequate vascular leakage/perfusion, local tubular inflammation and cell cycle arrest [4]. Of these factors, significant tissue inflammation in the kidney appears to be a critical mediator of sepsis-induced AKI [5]. Recent studies have indicated that innate immunity and inflammatory signaling pathways are involved in the pathogenesis of septic AKI, and these processes are initiated a few hours after injury by the infiltration of immune cells from the kidney and are of central importance to kidney regeneration [6,7]. We investigate the association of HBP with M1 macrophages in sepsis-induced AKI
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