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

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

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Title: Protection from septic peritonitis by rapid neutrophil recruitment through omental high endothelial venules
Author: Buscher, Konrad; Wang, Huiyu; Zhang, Xueli; Striewski, Paul; Wirth, Benedikt; Saggu, Gurpanna; Lütke-Enking, Stefan; Mayadas, Tanya N.; Ley, Klaus; Sorokin, Lydia; Song, Jian

Note: Order does not necessarily reflect citation order of authors.

Citation: Buscher, 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.
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Abstract: 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.
Published Version: doi:10.1038/ncomms10828
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4785224/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:26318516
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