
In Vivo Characterization of Neutrophil Extracellular Traps in Various Organs of a Murine Sepsis Model
Author(s) -
Koji Tanaka,
Yuhki Koike,
Takaya Shimura,
Masato Okigami,
Shozo Ide,
Yuji Toiyama,
Yoshinaga Okugawa,
Yasuhiro Inoue,
Toshimitsu Araki,
Keiichi Uchida,
Yasuhiko Mohri,
Akira Mizoguchi,
Masato Kusunoki
Publication year - 2014
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0111888
Subject(s) - neutrophil extracellular traps , platelet , sepsis , microcirculation , extracellular , endothelium , pathology , immunology , endothelial stem cell , platelet activation , microvessel , intravital microscopy , in vivo , lung , inflammation , chemistry , biology , medicine , microbiology and biotechnology , biochemistry , in vitro , endocrinology , immunohistochemistry
Neutrophil extracellular traps (NETs) represent extracellular microbial trapping and killing. Recently, it has been implicated in thrombogenesis, autoimmune disease, and cancer progression. The aim of this study was to characterize NETs in various organs of a murine sepsis model in vivo and to investigate their associations with platelets, leukocytes, or vascular endothelium. NETs were classified as two distinct forms; cell-free NETs that were released away from neutrophils and anchored NETs that were anchored to neutrophils. Circulating cell-free NETs were characterized as fragmented or cotton-like structures, while anchored NETs were characterized as linear, reticular, membranous, or spot-like structures. In septic mice, both anchored and cell-free NETs were significantly increased in postcapillary venules of the cecum and hepatic sinusoids with increased leukocyte-endothelial interactions. NETs were also observed in both alveolar space and pulmonary capillaries of the lung. The interactions of NETs with platelet aggregates, leukocyte-platelet aggregates or vascular endothelium of arterioles and venules were observed in the microcirculation of septic mice. Microvessel occlusions which may be caused by platelet aggregates or leukocyte-platelet aggregates and heterogeneously decreased blood flow were also observed in septic mice. NETs appeared to be associated with the formation of platelet aggregates or leukocyte-platelet aggregates. These observational findings may suggest the adverse effect of intravascular NETs on the host during a sepsis.