Endotoxin and Innate Immunity
Online ISSN : 2434-1177
Periodontal bacteria-induced neutrophil extracellular traps enhances proinflammatory responses in human endothelial cells
Hiroyuki TadaTakashi NishiokaKenji MatsushitaSakura OnoueKazuyoshi Kawahara
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2018 Volume 21 Pages 66-69

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Abstract

 In the inflammatory disease chronic periodontitis, the periodontium is exposed to a high density and diversity of periodontal bacteria. Neutrophils are the first line of defense in the periodontium. Circulating neutrophils adhere to endothelial cells by adhesion molecules, such as β2-integrin, following their migration across endothelial cells into the inflamed periodontium. Endothelial cell-derived developmental endothelial locus-1 (Del-1) acts as a negative regulator of neutrophil extravasation that inhibits β2-integrin-dependent adhesion to vascular endothelial cells. Neutrophil extracellular traps (NETs) are extracellular web-like DNA structures that contain bactericidal substances such as histones, human neutrophil elastase, and cathelicidin antimicrobial peptides. NETs are produced by many bacterial species, but it remains unknown whether the development of periodontal disease is due to periodontal bacteria-induced NET production. Fusobacterium nucleatum is a Gram-negative anaerobic bacterium associated with periodontal disease. We examined the effects of F. nucleatum-induced NET stimulation on the induction of Del-1 in human endothelial cells. A transendothelial migration assay was performed to evaluate the number of transmigrated neutrophils. Stimulation of human umbilical vein endothelial cells (HUVECs) with F. nucleatum-infected NET fragments enhanced the transendothelial migration of neutrophils. Furthermore, the Del-1 production induced by HUVECs was attenuated in NET fragments-primed cells. Thus, F. nucleatum-induced NETs may enhance neutrophil extravasation in a manner dependent on the attenuation of Del-1 production in endothelial cells. This study suggests that NETs are associated with the pathogenesis of periodontal disease.

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© 2018 Japanese Endotoxin and Innate Immunity Society
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