Gut Microbiota Restricts NETosis in Acute Mesenteric Ischemia-Reperfusion Injury.
Animals
Bacillus subtilis
/ pathogenicity
Cell Adhesion
Cells, Cultured
Disease Models, Animal
Escherichia coli
/ pathogenicity
Extracellular Traps
/ metabolism
Female
Gastrointestinal Microbiome
Germ-Free Life
Host-Pathogen Interactions
Leukocyte Rolling
Leukocytes
/ metabolism
Male
Mesenteric Ischemia
/ metabolism
Mesentery
/ blood supply
Mice, Inbred C57BL
Mice, Knockout
Neutrophil Infiltration
Neutrophils
/ metabolism
Reperfusion Injury
/ metabolism
Signal Transduction
Toll-Like Receptor 4
/ genetics
Venules
/ metabolism
extracellular traps
interferons
lipopolysaccharide
neutrophils
venules
Journal
Arteriosclerosis, thrombosis, and vascular biology
ISSN: 1524-4636
Titre abrégé: Arterioscler Thromb Vasc Biol
Pays: United States
ID NLM: 9505803
Informations de publication
Date de publication:
09 2020
09 2020
Historique:
pubmed:
3
7
2020
medline:
8
10
2020
entrez:
3
7
2020
Statut:
ppublish
Résumé
Recruitment of neutrophils and formation of neutrophil extracellular traps (NETs) contribute to lethality in acute mesenteric infarction. To study the impact of the gut microbiota in acute mesenteric infarction, we used gnotobiotic mouse models to investigate whether gut commensals prime the reactivity of neutrophils towards formation of neutrophil extracellular traps (NETosis). Approach and Results: We applied a mesenteric ischemia-reperfusion (I/R) injury model to germ-free (GF) and colonized C57BL/6J mice. By intravital imaging, we quantified leukocyte adherence and NET formation in I/R-injured mesenteric venules. Colonization with gut microbiota or monocolonization with Collectively, our results identified that the gut microbiota suppresses NETing neutrophil hyperreactivity in mesenteric I/R injury, while ensuring immunovigilance by enhancing neutrophil recruitment.
Identifiants
pubmed: 32611241
doi: 10.1161/ATVBAHA.120.314491
pmc: PMC7484055
mid: NIHMS1605423
doi:
Substances chimiques
Tlr4 protein, mouse
0
Toll-Like Receptor 4
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2279-2292Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL139641
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL141513
Pays : United States
Commentaires et corrections
Type : CommentIn
Type : CommentIn
Type : CommentIn
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