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Role of M2 Macrophages in Sepsis-Induced Acute Kidney Injury
Xing Li1, Genhua Mu1, Chunmei Song2
1Department of ICU, Yancheng City No. 1 People's Hospital, Yancheng, China.
Background:
Sepsis is a major cause of acute kidney injury (AKI), with high rates of morbidity and mortality. M2 macrophages have been shown to play important roles in the secretion of anti-inflammatory and tissue repair mediators. In this study, we investigate the role of M2 macrophages in sepsis-induced AKI by depleting these cells in vivo through the systemic administration of liposomal clodronate (LC).
Methods:
Male Sprague-Dawley rats were subjected to cecal ligation and puncture (CLP) or sham surgery. Biochemical and histological renal damage was assessed. Macrophage infiltration and M2 macrophage depletion were assessed by immunohistochemistry. RT-PCR was used to investigate the expression of the inducible nitric oxide synthase (iNOS), arginase 1 (Arg-1), and found in inflammatory zone 1 (FIZZ1) mRNAs. Western blots were performed to assay the tissue levels of interleukin-10 (IL-10) and tumor necrosis factor alpha (TNF-α).
Results:
M2 macrophages were obviously detected 72 h after sepsis-induced AKI. Kidney injury was more severe, renal function was decreased, and blood creatinine and blood urea nitrogen (BUN) levels were higher after M2 macrophage depletion. M2 macrophage depletion significantly inhibited the proliferation of tubular cells. M2 macrophage depletion also downregulated IL-10 expression and increased TNF-α secretion during sepsis-induced AKI.
Conclusions:
M2 macrophages attenuate sepsis-induced AKI, presumably by upregulating IL-10 expression and suppressing TNF-α secretion.
Insights
Depleting M2 macrophages worsens sepsis-induced acute kidney injury (AKI). These macrophages attenuate kidney damage by increasing anti-inflammatory IL-10 and reducing pro-inflammatory TNF-α.
Area of Science:
- Immunology
- Nephrology
- Pathophysiology
Background:
- Sepsis is a leading cause of acute kidney injury (AKI), characterized by high morbidity and mortality.
- M2 macrophages are recognized for their roles in producing anti-inflammatory and tissue-repair mediators.
- This study explores the protective function of M2 macrophages in sepsis-induced AKI.
Purpose of the Study:
- To investigate the role of M2 macrophages in the context of sepsis-induced AKI.
- To determine the impact of M2 macrophage depletion on renal function and injury markers.
- To elucidate the molecular mechanisms by which M2 macrophages influence sepsis-related kidney damage.
Main Methods:
- Sepsis was induced in male Sprague-Dawley rats via cecal ligation and puncture (CLP).
- M2 macrophages were systemically depleted using liposomal clodronate.
- Renal damage, macrophage infiltration, and gene/protein expression (iNOS, Arg-1, FIZZ1, IL-10, TNF-α) were assessed.
Main Results:
- M2 macrophages were present 72 hours post-sepsis.
- Depletion of M2 macrophages exacerbated kidney injury, decreased renal function, and elevated creatinine and BUN levels.
- M2 macrophage depletion inhibited tubular cell proliferation and altered cytokine profiles, downregulating IL-10 and upregulating TNF-α.
Conclusions:
- M2 macrophages play a protective role in attenuating sepsis-induced AKI.
- This protective effect is likely mediated through the upregulation of IL-10 and suppression of TNF-α.
- Targeting M2 macrophages may offer a therapeutic strategy for sepsis-induced AKI.
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