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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Front+Immunol
2016 ; 7
(ä): 484
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English Wikipedia
Neutrophils Discriminate between Lipopolysaccharides of Different Bacterial
Sources and Selectively Release Neutrophil Extracellular Traps
#MMPMID27867387
Pieterse E
; Rother N
; Yanginlar C
; Hilbrands LB
; van der Vlag J
Front Immunol
2016[]; 7
(ä): 484
PMID27867387
show ga
The release of neutrophil extracellular traps (NETs), either during "suicidal" or
"vital" NETosis, represents an important strategy of neutrophils to combat
Gram-negative bacteria. Lipopolysaccharide (LPS), a major component of the outer
membrane of Gram-negative bacteria, is a reported stimulus for NET formation.
Although it is widely acknowledged that the structural diversity in LPS
structures can elicit heterogeneous immune responses, species- and
serotype-specific differences in the capacity of LPS to trigger NET formation
have not yet been investigated. In the present study, we compared the
NET-inducing potential of LPS derived from Escherichia coli (serotypes O55:B5,
O127:B8, O128:B12, O111:B4, and O26:B6), Salmonella enterica (serotype
enteritidis), and Pseudomonas aeruginosa (serotype 10), under platelet-free and
platelet-rich conditions in vitro, and in whole blood ex vivo. Here, we
demonstrate that under serum- and platelet-free conditions, mimicking tissue
circumstances, neutrophils discriminate between LPS of different bacterial
sources and selectively release NETs only in response to LPS derived from E. coli
O128:B12 and P. aeruginosa 10, which both induced "suicidal" NETosis in an
autophagy- and reactive oxygen species (ROS)-dependent, but TLR4-independent
manner. Intriguingly, in whole blood cultures ex vivo, or in vitro in the
presence of platelets, all LPS serotypes induced "vital" NET formation. This
platelet-dependent release of NETs occurred rapidly without neutrophil cell death
and was independent from ROS formation and autophagy but required platelet TLR4
and CD62P-dependent platelet-neutrophil interactions. Taken together, our data
reveal a complex interplay between neutrophils and LPS, which can induce both
"suicidal" and "vital" NETosis, depending on the bacterial origin of LPS and the
presence or absence of platelets. Our findings suggest that LPS sensing by
neutrophils may be a critical determinant for restricting NET release to certain
Gram-negative bacteria only, which in turn may be crucial for minimizing
unnecessary NET-associated immunopathology.