
IndraLab
Statements
Lipopolysaccharide inhibits IFNB1. 40 / 40
|
3
37
reach
"Thus, the Cpb1-C3-C3aR signaling axis of the complement system represents an important amplification mechanism for pro inflammatory signaling and caspase-11-mediated cell death during infectious disease.In contrast to the role of complement in amplifying caspase-11 expression during murine sepsis models [26], prostaglandin E 2 (PGE 2) is capable of potently inhibiting LPS induced IFNbeta production in murine BMDMs, which has the subsequent effect of significantly impairing LPS mediated caspase-11 expression [38]."
reach
"These results suggested that 2-AP inhibited LPS induced IFN-beta production by preventing Toll/IL -1 receptor domain containing adaptor inducing IFN-beta (TRIF)-dependent signaling rather than myeloid differentiation factor (MyD) 88 dependent signaling, resulting in the inhibition of NO production."