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2017 ; 7
(ä): 138
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Ectodomain Shedding by ADAM17: Its Role in Neutrophil Recruitment and the
Impairment of This Process during Sepsis
#MMPMID28487846
Mishra HK
; Ma J
; Walcheck B
Front Cell Infect Microbiol
2017[]; 7
(ä): 138
PMID28487846
show ga
Neutrophils are specialized at killing bacteria and are recruited from the blood
in a rapid and robust manner during infection. A cascade of adhesion events
direct their attachment to the vascular endothelium and migration into the
underlying tissue. A disintegrin and metalloproteinase 17 (ADAM17) functions in
the cell membrane of neutrophils and endothelial cells by cleaving its
substrates, typically in a cis manner, at an extracellular site proximal to the
cell membrane. This process is referred to as ectodomain shedding and it results
in the downregulation of various adhesion molecules and receptors, and the
release of immune regulating factors. ADAM17 sheddase activity is induced upon
cell activation and rapidly modulates intravascular adhesion events in response
to diverse environmental stimuli. During sepsis, an excessive systemic
inflammatory response against infection, neutrophil migration becomes severely
impaired. This involves ADAM17 as indicated by increased levels of its cleaved
substrates in the blood of septic patients, and that ADAM17 inactivation improves
neutrophil recruitment and bacterial clearance in animal models of sepsis.
Excessive ADAM17 sheddase activity during sepsis thus appears to undermine in a
direct and indirect manner the necessary balance between intravascular adhesion
and de-adhesion events that regulate neutrophil migration into sites of
infection. This review provides an overview of ADAM17 function and regulation and
its potential contribution to neutrophil dysfunction during sepsis.
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