2017
DOI: 10.1189/jlb.3a0916-388rr
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TNF induces neutrophil adhesion via formin-dependent cytoskeletal reorganization and activation of β-integrin function

Abstract: Although essential for inflammatory responses, leukocyte recruitment to blood vessel walls in response to inflammatory stimuli, such as TNF-, can contribute to vascular occlusion in inflammatory diseases, including atherosclerosis. We aimed to further characterize the mechanisms by which TNF stimulates adhesive and morphologic alterations in neutrophils.

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Cited by 29 publications
(15 citation statements)
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“…The cytokine response of TNF‐α elevation observed after S. elongatus injection was not statistically significant but nevertheless noteworthy. This cytokine typically increases in the setting of inflammation and is crucial for neutrophil migration and adhesion (Silveira et al ., 2018). Its increase 4 h following S. elongatus injection preceded the increase in neutrophils seen 48 h after injection in these rats.…”
Section: Discussionmentioning
confidence: 99%
“…The cytokine response of TNF‐α elevation observed after S. elongatus injection was not statistically significant but nevertheless noteworthy. This cytokine typically increases in the setting of inflammation and is crucial for neutrophil migration and adhesion (Silveira et al ., 2018). Its increase 4 h following S. elongatus injection preceded the increase in neutrophils seen 48 h after injection in these rats.…”
Section: Discussionmentioning
confidence: 99%
“…While TNF-a has not been directly implicated in this polarization, its role in TGF-b pathway and the other pathways in which it modulates neutrophil activity described below highlights the importance of neutrophil-neoplasm interaction. In normal vasculature in vivo, TNF-a increases neutrophil recruitment and endothelial adhesion via cytoskeletal remodeling (96,97). TNF-a also has a "priming" effect on neutrophils, causing them to be more responsive to stimuli (98).…”
Section: Neutrophilsmentioning
confidence: 99%
“…This cytokine is suggested to be generated as an early consequence of ischemia-reperfusion [207] and has potent effects on both leukocytes and endothelial cells. In neutrophils, TNF-α stimulates the surface expression of β−2 integrins [208], in turn augmenting their adhesion to the blood vessel wall [208] and interactions with other cells via NF-κB and MAPK signaling [209]. Furthermore, TNF-α degrades the endothelial glycocalyx (shown to be reduced in SCD patients) [210, 211], alters endothelium-derived NO bioavailability [212] and upregulates adhesion molecule expression on the endothelium [213], with a monocyte-dependent TNF-endothelial activation axis being recently described in sickle mice [207].…”
Section: Chronic Inflammatory Mechanisms In Sickle Cell Diseasementioning
confidence: 99%