Payen et al. reported that, in patients with septic shock, mRNA S100A12 expression by circulating leukocytes was decreased during the recovery phase [46] . One possible function of S100A12 in host defense during infection and sepsis is its role as a DAMP. NF-κB mediated expression of pro-infl ammatory cytokines and upregulation of ICAM-1 and vascular cell adhesion molecule (VCAM)-1 on endothelium has been documen ted in vitro after S100A12 stimulation [47] . Furthermore, S100A12 could be of benefi t for the host during infection and sepsis due to its (more direct) antibacterial activity. Cole et al. determined that S100A12 has activity primarily against Gram-negative bacteria, including E. coli [48] . Because of the absence of S100A12 in rodents, a potential functional role of S100A12 during sepsis cannot be easily investigated by inhibiting/deleting S100A12 in animals. Altogether, the role of S100A12 during sepsis has yet to be evaluated using non-rodent models.