Abstract
Neutrophil is a major player in the pathophysiology of severe sepsis. Recent studies have revealed that the cell death mechanism of neutrophils directly relates to the development of organ dysfunction during sepsis. Here we discuss about the different types of neutrophil cell death such as necrosis, apoptosis, autophagy, and the unique cell death style dubbed NETosis. NETosis cells release neutrophil extracellular traps (NETs), which are composed of chromatin bound to granular and nucleic proteins. The primary purpose of NET release is thought to be the control of microbial infections; however, it acts as a danger signal for the host as well. The harmful substances such as DNA, histones, and high-mobility group box 1 (HMGB1) and many other danger-associated molecular patterns (DAMPs) released along with NETosis or from necrotic neutrophils also contribute to the pathogenesis of sepsis. At the same time, the coagulation system, which is closely tied to these neutrophil cell death mechanisms, is often over-activated. It is well known that individual bacterial pathogens express virulence factors that modulate cell death pathways and influence the coagulation disorder during sepsis. Moreover, extensive cross talk exists between these two phenomena, whereby inflammation leads to activation of coagulation and coagulation considerably affects inflammatory activity. A greater knowledge of cell death pathways in sepsis informs the potential for future therapies designed to ameliorate excessive immune responses during sepsis.
Highlights
Neutrophil is a major player in the pathophysiology of severe sepsis
We introduce the mechanism and the morphological findings of major types of neutrophil deaths in the following part
Neutrophil cell death plays a pivotal role in the pathophysiology of sepsis
Summary
Neutrophil cell death plays a pivotal role in the pathophysiology of sepsis. Apoptosis has been the major focus of investigation, necrosis, autophagic cell death, and the new comer NETosis play significant roles in this critical situation. A variety of styles of cell death coexist in sepsis, and the population of necrosis and NETosis are especially important to regulate the host condition. It is apparent that cell disintegration and molecules such as histones, nucleosomes, proteases, and tissue factor released from the dead cells all play governing roles in the inflammatory and coagulatory responses, host immune competence, during sepsis. Authors’ contributions TI, NH, and IN wrote the manuscript. MM edited the manuscript as a native English speaker. All the authors read and approved the final manuscript
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