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10.1038/ncomms10828

http://scihub22266oqcxt.onion/10.1038/ncomms10828
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C4785224!4785224!26940548
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suck abstract from ncbi


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pmid26940548      Nat+Commun 2016 ; 7 (ä): ä
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  • Protection from septic peritonitis by rapid neutrophil recruitment through omental high endothelial venules #MMPMID26940548
  • Buscher K; Wang H; Zhang X; Striewski P; Wirth B; Saggu G; Lütke-Enking S; Mayadas TN; Ley K; Sorokin L; Song J
  • Nat Commun 2016[]; 7 (ä): ä PMID26940548show ga
  • 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 TNF?-, 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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