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Nat Commun. 2016 Mar 4;7:10828. doi: 10.1038/ncomms10828.

Protection from septic peritonitis by rapid neutrophil recruitment through omental high endothelial venules.

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Institute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster 48149, Germany.
Cells-in-Motion Cluster of Excellence, University of Muenster, Muenster 48149, Germany.
Department of Nephrology and Rheumatology, University of Muenster, Muenster 48149, Germany.
Institute for Computational and Applied Mathematics, University of Muenster, Muenster 48149, Germany.
Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Division of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.


Acute 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.

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