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	[104–108]
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	[111, 113, 114]
Endotoxemia	sST2 reduces LPS-mediated mortality and inhibits LPS-induced proinflammatory cytokines	[115–117]
Endotoxemia	sST2 reduces inflammatory cell infiltration and vascular leakage, and suppresses proinflammatory cytokine production in lung tissues	[120, 121]
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	[125, 126]
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]