Table 1 Roles of IL-33/ST2 in sepsis models
Disease | Role of IL-33/ST2 | Referenced |
|---|---|---|
Sepsis | Sepsis patients have higher levels of serum IL-33 and sST2 | |
Endotoxemia | ST2 negatively regulates TLR4 signaling and maintains LPS tolerance | [109] |
Endotoxemia | ST2 negatively regulates TLR2 signaling, but is not required for BLP tolerance | [110] |
Endotoxemia | IL-33 enhances LPS-induced proinflammatory mediators in mouse macrophages in a ST2-dependent manner | |
Endotoxemia | sST2 reduces LPS-mediated mortality and inhibits LPS-induced proinflammatory cytokines | |
Endotoxemia | sST2 reduces inflammatory cell infiltration and vascular leakage, and suppresses proinflammatory cytokine production in lung tissues | |
Abdominal sepsis | ST2 deletion protects mice challenged with secondary pneumonia | [122] |
Abdominal sepsis | ST2 deficiency increases the susceptibility to sepsis | [123] |
Streptococcus pneumoniae infection | ST2 deficiency protects mice challenged with S. pneumonia | [124] |
Abdominal sepsis | IL-33 enhances neutrophil recruitment and protects mice with more efficient bacterial clearance and improved survival | |
Abdominal sepsis | IL-33 administration attenuates organ damage in the late phase of sepsis | [126] |
Staphylococcus aureus infection | IL-33 administration facilitates neutrophil recruitment and bacterial clearance | [127] |