Abstract
Uncontrolled inflammatory and immune responses are often involved in the development of acute and chronic forms of renal injury. Neutrophils are innate immune cells recruited early to sites of inflammation, where they produce pro-inflammatory cytokines and release mesh-like structures comprised of DNA and granular proteins known as neutrophil extracellular traps (NETs). NETs are potentially toxic, contribute to glomerular injury, activate autoimmune processes, induce vascular damage, and promote kidney fibrosis. Evidence from multiple studies suggests that an imbalance between production and clearance of NETs is detrimental for renal health. Hence strategies aimed at modulating NET-associated processes could have a therapeutic impact on a myriad of inflammatory diseases that target the kidney. Here, we summarize the role of NETs in the pathogenesis of renal diseases and their mechanisms of tissue damage.
Highlights
Renal disease and the immune system are inextricably linked
The field of NETosis has grown exponentially since 2004 when Brinkmann V. et al described neutrophil extracellular traps (NETs) as extracellular fibers comprised of chromatin and granule proteins released by neutrophils and able to bind bacteria [9]
Though the conclusions drawn by these studies are as diverse as the studies themselves, it is evident that NETosis is more than a simple host-defense mechanism [9,13]
Summary
Renal disease and the immune system are inextricably linked. The kidneys are frequent targets of harmful immune responses that contribute to the development of acute forms of renal injury, as well as chronic kidney disease progression [1,2,3,4]. Activation of tissue repair mechanisms after an immune-mediated injury can lead to fibrosis and kidney failure [7]. Neutrophils are the first cellular effectors to be recruited at sites of infection and tissue damage; where they play a significant role in inflammation, immune cell recruitment, pathogen clearance, and tissue repair. Neutrophils execute their functions through four main mechanisms: phagocytosis, degranulation, cytokine production, and neutrophil extracellular trap (NET) formation [8,9]. We summarize the ongoing knowledge regarding NET-associated mechanisms of tissue kidney diseases (Figure 1). NETs produce tissue damage through DNA, histones, neutrophil elastase, autoantibodies and complement activation.
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