|
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]
|
