In fact, both peptides prevent endotoxic shock in a murine experimental model (17). Although our in vitro and in vivo studies using specific VIP agonists have indicated that the VPAC1 is the main mediator of the VIP and PACAP anti-inflammatory action (18), the role of PAC1 in inflammation remains undefined.
Full Answer
Sepsis and septic shock: pro-inflammatory or anti-inflammatory state? A considerable body of evidence indicates that together with an important pro-inflammatory reaction, a anti-inflammatory response contributes to the onset of sepsis and organ failure.
He M., Sun J., Zhang H., Bawa M. S., Bhatia M. (2006) Inflammatory mediators in sepsis: cytokines, chemokines, adhesion molecules and gases. J. Organ Dysfunction2, 80–92 [Google Scholar]
Based on these viewpoints, we suggest that replenishing the protective mediators that are down-regulated in sepsis, while withdrawing the elevated deleterious factors, may lead to the discovery of new therapies for improving survival in septic patients, a goal that has been elusive for decades.
Excessive neutrophil infiltration releases ROS and MPO, leading to multiple organ injuries. On the other hand, novel immunomodulatory substances attract neutrophils at the infectious area, promote bacterial clearance, attenuate systemic inflammation, reduce neutrophil infiltration at various organs, and improve survival in sepsis.