Figure 12. Schematic summary of signaling events in H2S-induced neurogenic inflammation in a murine model of polymicrobial sepsis.
H2S has been demonstrated to be overproduced in sepsis. H2S stimulation of TRPV1 and the downstream release of SP lead to the activation of ERK1/2, which subsequently induces the phosphorylation and degradation of IκBα, as well as the translocation and activation of NF-κB, thereby leading to SIRS and MODS characteristic of severe sepsis. indicates exogenous administration;
indicates inhibition.