3.3 Cell pyrosis
Pyrosis is currently defined as a specifically programmed cell death characterized by the release of inflammatory cytokines, which are involved in inflammation and immune response and can be activated by classical pathways dependent on caspase-1 or nonclassical pathways dependent on caspase-4/5/11 [33]. During sepsis, appropriate pyrosis is helpful to resist bacterial infection and reduce the damage to tissues and organs. However, excessive pyrosis will lead to further aggravation of infection and the emergence of multiple organ failure (MODS). IL-18/IL-1 can be reduced by inhibiting the activation of inflammatory corpuscles and regulating the pyrolytic activity of cells β To protect against multiple organ injury in sepsis. In addition, transcription factors are also involved in the regulation of cell death in sepsis, such as NF- κ B and nuclear factor red blood cell 2 related factors (Nrf2). Hu [34] et al. Confirmed by animal experiments that after prophylactic glutamine (Gln) supplementation in the septic mouse group, it can increase the cell apoptosis in the early stage of sepsis to enhance the bacterial clearance ability, and can reduce the cell apoptosis and reduce IL-1 in the late stage of sepsis β The release of inflammatory cytokines such as IL-18 can improve organ dysfunction in sepsis.