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Introduction: Neutrophils are important participants in the innate immune response. They rapidly and efficiently identify and clear infectious agents by expressing large numbers of membrane receptors. Upon tissue injury or pathogen invasion, neutrophils are the first immune cells to reach the site of injury and participate in the inflammatory response. Materials and methods: A thorough search on PubMed related to neutrophil death or clearance pathways was performed. Conclusion: Inflammatory response and tissue damage can be aggravated when neutrophils are not removed rapidly from the site of injury. Recent studies have shown that neutrophils can be cleared through a variety of pathways, including non-inflammatory and inflammatory death, as well as reverse migration. Non-inflammatory death pathways include apoptosis and autophagy. Inflammatory death pathways include necroptosis, pyroptosis and NETosis. This review highlights the basic properties of neutrophils and the impact of their clearance pathways on the inflammatory response. [ABSTRACT FROM AUTHOR]

Deep hypothermic circulatory arrest (DHCA) has been widely used in the operations involving the aortic arch and brain aneurysm since 1950s; but prolonged DHCA contributes significantly to neurological deficit which remains a major cause of postoperative morbidity and mortality. It has been reported that hydrogen exerts a therapeutic antioxidant activity by selectively reducing hydroxyl radical. In this study, DHCA treated rats developed a significant oxidative stress, inflammatory reaction and apoptosis. The administration of HRS resulted in a significant decrease in the brain injury, together with lower production of IL-1β, TNF-α, 8-OHdG and MDA as well as decreased activity of NOS while increased activity of SOD. The apoptotic index as well as the expressions of caspase-3 in brain tissue was significantly decreased after treatment. HRS administration significantly attenuated the severity of DHCA induced brain injury by mechanisms involving amelioration of oxidative stress, down-regulation of inflammatory factors and reduction of apoptosis. [ABSTRACT FROM AUTHOR]