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Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice

Tumor necrosis factor-α (TNF-α) is a key factor for the pathogenesis of inflammatory bowel diseases (IBD), whose function is known to be mediated by TNF receptor 1 (TNFR1) or 2. However, the precise role of the two receptors in IBD remains poorly understood. Herein, acute colitis was induced by dext...

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Autores principales: Wang, Ke, Han, Gencheng, Dou, Yan, Wang, Yi, Liu, Guijun, Wang, Renxi, Xiao, He, Li, Xinying, Hou, Chunmei, Shen, Beifen, Guo, Renfeng, Li, Yan, Shi, Yanchun, Chen, Guojiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3532169/
https://www.ncbi.nlm.nih.gov/pubmed/23285227
http://dx.doi.org/10.1371/journal.pone.0052924
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author Wang, Ke
Han, Gencheng
Dou, Yan
Wang, Yi
Liu, Guijun
Wang, Renxi
Xiao, He
Li, Xinying
Hou, Chunmei
Shen, Beifen
Guo, Renfeng
Li, Yan
Shi, Yanchun
Chen, Guojiang
author_facet Wang, Ke
Han, Gencheng
Dou, Yan
Wang, Yi
Liu, Guijun
Wang, Renxi
Xiao, He
Li, Xinying
Hou, Chunmei
Shen, Beifen
Guo, Renfeng
Li, Yan
Shi, Yanchun
Chen, Guojiang
author_sort Wang, Ke
collection PubMed
description Tumor necrosis factor-α (TNF-α) is a key factor for the pathogenesis of inflammatory bowel diseases (IBD), whose function is known to be mediated by TNF receptor 1 (TNFR1) or 2. However, the precise role of the two receptors in IBD remains poorly understood. Herein, acute colitis was induced by dextran sulfate sodium (DSS) instillation in TNFR1 or 2−/− mice. TNFR1 ablation led to exacerbation of signs of colitis, including more weight loss, increased mortality, colon shortening and oedema, severe intestinal damage, and higher levels of myeloperoxidase compared to wild-type counterparts. While, TNFR2 deficiency had opposite effects. This discrepancy was reflected by alteration of proinflammatory cytokine and chemokine production in the colons. Importantly, TNFR1 ablation rendered enhanced apoptosis of colonic epithelial cells and TNFR2 deficiency conferred pro-apoptotic effects of lamina propria (LP)-immune cells, as shown by the decreased ratio of Bcl-2/Bax and enhanced nuclear factor (NF)-κB activity.
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spelling pubmed-35321692013-01-02 Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice Wang, Ke Han, Gencheng Dou, Yan Wang, Yi Liu, Guijun Wang, Renxi Xiao, He Li, Xinying Hou, Chunmei Shen, Beifen Guo, Renfeng Li, Yan Shi, Yanchun Chen, Guojiang PLoS One Research Article Tumor necrosis factor-α (TNF-α) is a key factor for the pathogenesis of inflammatory bowel diseases (IBD), whose function is known to be mediated by TNF receptor 1 (TNFR1) or 2. However, the precise role of the two receptors in IBD remains poorly understood. Herein, acute colitis was induced by dextran sulfate sodium (DSS) instillation in TNFR1 or 2−/− mice. TNFR1 ablation led to exacerbation of signs of colitis, including more weight loss, increased mortality, colon shortening and oedema, severe intestinal damage, and higher levels of myeloperoxidase compared to wild-type counterparts. While, TNFR2 deficiency had opposite effects. This discrepancy was reflected by alteration of proinflammatory cytokine and chemokine production in the colons. Importantly, TNFR1 ablation rendered enhanced apoptosis of colonic epithelial cells and TNFR2 deficiency conferred pro-apoptotic effects of lamina propria (LP)-immune cells, as shown by the decreased ratio of Bcl-2/Bax and enhanced nuclear factor (NF)-κB activity. Public Library of Science 2012-12-28 /pmc/articles/PMC3532169/ /pubmed/23285227 http://dx.doi.org/10.1371/journal.pone.0052924 Text en © 2012 Wang et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Wang, Ke
Han, Gencheng
Dou, Yan
Wang, Yi
Liu, Guijun
Wang, Renxi
Xiao, He
Li, Xinying
Hou, Chunmei
Shen, Beifen
Guo, Renfeng
Li, Yan
Shi, Yanchun
Chen, Guojiang
Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice
title Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice
title_full Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice
title_fullStr Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice
title_full_unstemmed Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice
title_short Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice
title_sort opposite role of tumor necrosis factor receptors in dextran sulfate sodium-induced colitis in mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3532169/
https://www.ncbi.nlm.nih.gov/pubmed/23285227
http://dx.doi.org/10.1371/journal.pone.0052924
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