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Tissue factor: a mediator of inflammatory cell recruitment, tissue injury, and thrombus formation in experimental colitis
There is growing evidence for an interplay between inflammatory and coagulation pathways in acute and chronic inflammatory diseases. However, it remains unclear whether components of the coagulation pathway, such as tissue factor (TF), contribute to intestinal inflammation, and whether targeting TF...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2007
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118639/ https://www.ncbi.nlm.nih.gov/pubmed/17562818 http://dx.doi.org/10.1084/jem.20062354 |
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author | Anthoni, Christoph Russell, Janice Wood, Katherine C. Stokes, Karen Y. Vowinkel, Thorsten Kirchhofer, Daniel Granger, D. Neil |
author_facet | Anthoni, Christoph Russell, Janice Wood, Katherine C. Stokes, Karen Y. Vowinkel, Thorsten Kirchhofer, Daniel Granger, D. Neil |
author_sort | Anthoni, Christoph |
collection | PubMed |
description | There is growing evidence for an interplay between inflammatory and coagulation pathways in acute and chronic inflammatory diseases. However, it remains unclear whether components of the coagulation pathway, such as tissue factor (TF), contribute to intestinal inflammation, and whether targeting TF will blunt the inflammatory cell recruitment, tissue injury, and enhanced thrombus formation that occur in experimental colitis. Mice were fed 3% dextran sodium sulfate (DSS) to induce colonic inflammation, with some mice receiving a mouse TF-blocking antibody (muTF-Ab). The adhesion of leukocytes and platelets in colonic venules, light/dye-induced thrombus formation in cremaster muscle microvessels, as well as disease activity index, thrombin–antithrombin (TAT) complexes in plasma, and histopathologic changes in the colonic mucosa were monitored in untreated and muTF-Ab–treated colitic mice. In untreated mice, DSS elicited the recruitment of adherent leukocytes and platelets in colonic venules, caused gross and histologic injury, increased plasma TAT complexes, and enhanced thrombus formation in muscle arterioles. muTF-Ab prevented elevation in TAT complexes, reduced blood cell recruitment and tissue injury, and blunted thrombus formation in DSS colitic mice. These findings implicate TF in intestinal inflammation and support an interaction between inflammation and coagulation in experimental colitis. |
format | Text |
id | pubmed-2118639 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21186392008-01-09 Tissue factor: a mediator of inflammatory cell recruitment, tissue injury, and thrombus formation in experimental colitis Anthoni, Christoph Russell, Janice Wood, Katherine C. Stokes, Karen Y. Vowinkel, Thorsten Kirchhofer, Daniel Granger, D. Neil J Exp Med Articles There is growing evidence for an interplay between inflammatory and coagulation pathways in acute and chronic inflammatory diseases. However, it remains unclear whether components of the coagulation pathway, such as tissue factor (TF), contribute to intestinal inflammation, and whether targeting TF will blunt the inflammatory cell recruitment, tissue injury, and enhanced thrombus formation that occur in experimental colitis. Mice were fed 3% dextran sodium sulfate (DSS) to induce colonic inflammation, with some mice receiving a mouse TF-blocking antibody (muTF-Ab). The adhesion of leukocytes and platelets in colonic venules, light/dye-induced thrombus formation in cremaster muscle microvessels, as well as disease activity index, thrombin–antithrombin (TAT) complexes in plasma, and histopathologic changes in the colonic mucosa were monitored in untreated and muTF-Ab–treated colitic mice. In untreated mice, DSS elicited the recruitment of adherent leukocytes and platelets in colonic venules, caused gross and histologic injury, increased plasma TAT complexes, and enhanced thrombus formation in muscle arterioles. muTF-Ab prevented elevation in TAT complexes, reduced blood cell recruitment and tissue injury, and blunted thrombus formation in DSS colitic mice. These findings implicate TF in intestinal inflammation and support an interaction between inflammation and coagulation in experimental colitis. The Rockefeller University Press 2007-07-09 /pmc/articles/PMC2118639/ /pubmed/17562818 http://dx.doi.org/10.1084/jem.20062354 Text en Copyright © 2007, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Anthoni, Christoph Russell, Janice Wood, Katherine C. Stokes, Karen Y. Vowinkel, Thorsten Kirchhofer, Daniel Granger, D. Neil Tissue factor: a mediator of inflammatory cell recruitment, tissue injury, and thrombus formation in experimental colitis |
title | Tissue factor: a mediator of inflammatory cell recruitment, tissue injury, and thrombus formation in experimental colitis |
title_full | Tissue factor: a mediator of inflammatory cell recruitment, tissue injury, and thrombus formation in experimental colitis |
title_fullStr | Tissue factor: a mediator of inflammatory cell recruitment, tissue injury, and thrombus formation in experimental colitis |
title_full_unstemmed | Tissue factor: a mediator of inflammatory cell recruitment, tissue injury, and thrombus formation in experimental colitis |
title_short | Tissue factor: a mediator of inflammatory cell recruitment, tissue injury, and thrombus formation in experimental colitis |
title_sort | tissue factor: a mediator of inflammatory cell recruitment, tissue injury, and thrombus formation in experimental colitis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118639/ https://www.ncbi.nlm.nih.gov/pubmed/17562818 http://dx.doi.org/10.1084/jem.20062354 |
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