Buscher, KonradWang, HuiyuZhang, XueliStriewski, PaulWirth, BenediktSaggu, GurpannaLütke-Enking, StefanMayadas, TanyaLey, KlausSorokin, LydiaSong, Jian2016-04-012016Buscher, K., H. Wang, X. Zhang, P. Striewski, B. Wirth, G. Saggu, S. Lütke-Enking, et al. 2016. “Protection from septic peritonitis by rapid neutrophil recruitment through omental high endothelial venules.” Nature Communications 7 (1): 10828. doi:10.1038/ncomms10828. http://dx.doi.org/10.1038/ncomms10828.2041-1723http://nrs.harvard.edu/urn-3:HUL.InstRepos:26318516Acute peritonitis is a frequent medical condition that can trigger severe sepsis as a life-threatening complication. Neutrophils are first-responders in infection but recruitment mechanisms to the abdominal cavity remain poorly defined. Here, we demonstrate that high endothelial venules (HEVs) of the greater omentum constitute a main entry pathway in TNFα-, Escherichia coli (E. coli)- and caecal ligation and puncture-induced models of inflammation. Neutrophil transmigration across HEVs is faster than across conventional postcapillary venules and requires a unique set of adhesion receptors including peripheral node addressin, E-, L-selectin and Mac-1 but not P-selectin or LFA-1. Omental milky spots readily concentrate intra-abdominal E. coli where macrophages and recruited neutrophils collaborate in phagocytosis and killing. Inhibition of the omental neutrophil response exacerbates septic progression of peritonitis. This data identifies HEVs as a clinically relevant vascular recruitment site for neutrophils in acute peritonitis that is indispensable for host defence against early systemic bacterial spread and sepsis.en-USJournal Article2016-04-0110.1038/ncomms10828