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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[Mar]; 7
(?): 10828
PMID26940548
show 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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