TLR4 and septic shock: Our previous study demonstrated that Fh12 activates macrophages into a non-inflammatory phenotype through TLR4 and, in doing so, functions as an LPS antagonist blocking the inflammatory mediators induced by LPS in vivo (in a murine model of septic shock)12 and in vitro, both in murine macrophages, and in human monocytes11, 12.