Sepsis is a systemic inflammatory syndrome caused by infection disorders. The core mechanism of sepsis is immune dysfunction. Neutrophils are the most abundant circulating white blood cells, which play a crucial role in mediating the innate immune response. Previous studies have shown that an effective way to treat sepsis is through the regulation of neutrophil functions. Autophagy, a highly conserved degradation process, is responsible for removing denatured proteins or damaged organelles within cells and protecting cells from external stimuli. It is a key homeostasis process that promotes neutrophil function and differentiation. Autophagy has been shown to be closely associated with inflammation and immunity. Neutrophils, the first line of innate immunity, migrate to inflammatory sites upon their activation. Neutrophil-mediated autophagy may participate in the clinical course of sepsis. In this review, we summarized and analyzed the latest research findings on the changes in neutrophil external traps during sepsis, the regulatory role of autophagy in neutrophil, and the potential application of autophagy-driven NETs in sepsis, so as to guide clinical treatment of sepsis.
Keywords: Autophagy; Molecular mechanism; Neutrophil extracellular trap; Prognostic marker; Sepsis.
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