Neutrophil extracellular traps in intracerebral hemorrhage: implications for pathogenesis and therapeutic targets

Intracerebral hemorrhage is a common neurological disease, and its pathological mechanism is complex. As the first recruited leukocyte subtype after intracerebral hemorrhage, neutrophils play an important role in tissue damage. In the past, it was considered that neutrophils performed their functions through phagocytosis, chemotaxis, and degranulation. In recent years, studies have found that neutrophils also have the function of secreting extracellular traps. Extracellular traps are fibrous structure composed of chromatin and granular proteins, which plays an important role in innate immunity. Studies have shown a large number of neutrophil extracellular traps in hematoma samples, plasma samples, and drainage samples after intracerebral hemorrhage. In this paper, we summarized the related mechanisms of neutrophil external traps and injury after intracerebral hemorrhage. Neutrophil extracellular traps are involved in the process of brain injury after intracerebral hemorrhage. The application of related inhibitors to inhibit the formation of neutrophil external traps or promote their dissolution can effectively alleviate the pathological damage caused by intracerebral hemorrhage.

Automated summary

Intracerebral hemorrhage is a common neurological disease with a complex pathological mechanism. Neutrophils, as the first recruited leukocyte subtype after intracerebral hemorrhage, play a crucial role in tissue damage. Previous beliefs regarded neutrophils' functions to be phagocytosis, chemotaxis, and degranulation. However, recent studies have revealed that neutrophils also secrete extracellular traps, which are fibrous structures consisting of chromatin and granular proteins, and play an important role in innate immunity. These extracellular traps have been found in abundance in hematoma samples, plasma samples, and drainage samples after intracerebral hemorrhage. This paper summarizes the mechanisms of neutrophil extracellular traps and the resulting injury following intracerebral hemorrhage and suggests that inhibiting their formation or promoting their dissolution can effectively alleviate the pathological damage caused by intracerebral hemorrhage.