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.