Neutrophils, as the first line in defending pathogens, are the most abundant cells in the peripheral blood cells. Normally, the lifespan of neutrophils is relatively short, with a half-life of 6-8h. Spontaneous apoptosis has been observed in isolated neutrophils in vitro. But under inflammatory insults, the spontaneous apoptosis of neutrophils is inhibited and the longevity of neutrophils will be increased to more than 48h. The increased lifespan of neutrophils may be helpful in pathogen clearance and tissue healing. But it will also result in some undesired side effects, such as systemic inflammation and organ injury, which are involved in multiple inflammatory or immunological diseases. Therefore, neutrophil apoptosis has been proposed to be a promising target against neutrophilic inflammatory responses in critical illness, including sepsis, acute respiratory distress syndrome, etc.
Despite the inhibited apoptosis, neutrophils may undergo some other forms of death in critical care settings. Programmed necrosis, also called necroptosis, can result in mitochondria release and initiate innate immune responses. The release of neutrophil extracellular trap (NET), a key mediator of inflammatory organ injury, is called NETosis, while some scientists suggest that NETosis can be only used when the neutrophil demise is obvious. Pyroptosis is another type of cell death, which is more related to the NET release from neutrophils because of the pore induced by activated Gasdermin D.
The goal of this research topic is to provide a forum to advance research on the clinical significance of neutrophil death dysregulation, the molecular mechanism of different types of neutrophil death in sepsis, trauma, burn, ischemia-reperfusion injury, and other critical illness induced by acute inflammatory responses, as well as clinical and preclinical interventions in an attempt to attenuate the inflammatory or immunological responses induced by abnormal death of neutrophils.
We welcome the submission of Original Research, Review articles, and Perspectives in this Research Topic, covering, but not limited to, the following sub-topics:
1) Biomarkers, phenotypes, clinical significance of the abnormal neutrophil death in critical settings;
2) Molecular mechanism of dysregulated neutrophil death in critical care settings, including apoptosis, necroptosis, NETosis, pyroptosis, ferroptosis, etc;
3) Shift of death types in neutrophils in critical care diseases;
4) Correlation of neutrophil death and other biological function of neutrophils;
5) The interaction of neutrophils undergoing different types of death with other cells.
Neutrophils, as the first line in defending pathogens, are the most abundant cells in the peripheral blood cells. Normally, the lifespan of neutrophils is relatively short, with a half-life of 6-8h. Spontaneous apoptosis has been observed in isolated neutrophils in vitro. But under inflammatory insults, the spontaneous apoptosis of neutrophils is inhibited and the longevity of neutrophils will be increased to more than 48h. The increased lifespan of neutrophils may be helpful in pathogen clearance and tissue healing. But it will also result in some undesired side effects, such as systemic inflammation and organ injury, which are involved in multiple inflammatory or immunological diseases. Therefore, neutrophil apoptosis has been proposed to be a promising target against neutrophilic inflammatory responses in critical illness, including sepsis, acute respiratory distress syndrome, etc.
Despite the inhibited apoptosis, neutrophils may undergo some other forms of death in critical care settings. Programmed necrosis, also called necroptosis, can result in mitochondria release and initiate innate immune responses. The release of neutrophil extracellular trap (NET), a key mediator of inflammatory organ injury, is called NETosis, while some scientists suggest that NETosis can be only used when the neutrophil demise is obvious. Pyroptosis is another type of cell death, which is more related to the NET release from neutrophils because of the pore induced by activated Gasdermin D.
The goal of this research topic is to provide a forum to advance research on the clinical significance of neutrophil death dysregulation, the molecular mechanism of different types of neutrophil death in sepsis, trauma, burn, ischemia-reperfusion injury, and other critical illness induced by acute inflammatory responses, as well as clinical and preclinical interventions in an attempt to attenuate the inflammatory or immunological responses induced by abnormal death of neutrophils.
We welcome the submission of Original Research, Review articles, and Perspectives in this Research Topic, covering, but not limited to, the following sub-topics:
1) Biomarkers, phenotypes, clinical significance of the abnormal neutrophil death in critical settings;
2) Molecular mechanism of dysregulated neutrophil death in critical care settings, including apoptosis, necroptosis, NETosis, pyroptosis, ferroptosis, etc;
3) Shift of death types in neutrophils in critical care diseases;
4) Correlation of neutrophil death and other biological function of neutrophils;
5) The interaction of neutrophils undergoing different types of death with other cells.
