Tumor necrosis factor-neuropeptide y cross talk regulates inflammation, epithelial barrier functions, and colonic motility
Inflammatory Bowel Diseases, ISSN: 1078-0998, Vol: 19, Issue: 12, Page: 2535-2546
2013
- 51Citations
- 61Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations51
- Citation Indexes51
- 51
- CrossRef24
- Captures61
- Readers61
- 61
Article Description
Background: Neuro-immune interactions play a significant role in regulating the severity of inflammation. Our previous work demonstrated that neuropeptide Y (NPY) is upregulated in the enteric nervous system during murine colitis and that NPY knockout mice exhibit reduced inflammation. Here, we investigated if NPY expression during inflammation is induced by tumor necrosis factor (TNF), the main proinflammatory cytokine. Methods: Using primary enteric neurons and colon explant cultures from wild type and NPY knockout (NPY) mice, we determined if NPY knockdown modulates TNF release and epithelial permeability. Further, we assessed if NPY expression is inducible by TNF in enteric neuronal cells and mouse model of experimental colitis, using the TNF inhibitors-etanercept (blocks transmembrane and soluble TNF) and XPro1595 (blocks soluble TNF only). Results: We found that enteric neurons express TNF receptors (TNFR1 and R2). Primary enteric neurons from NPY mice produced less TNF compared with wild type. Further, TNF activated NPY promoter in enteric neurons through phospho-c-Jun. NPY mice had decreased intestinal permeability. In vitro, NPY increased epithelial permeability through phosphatidyl inositol-3-kinase (PI3-K)-induced pore-forming claudin-2. TNF inhibitors attenuated NPY expression in vitro and in vivo. TNF inhibitor-treated colitic mice exhibited reduced NPY expression and inflammation, reduced oxidative stress, enhanced neuronal survival, and improved colonic motility. XPro1595 had more protective effects on neuronal survival and motility compared with etanercept. Conclusions: We demonstrate a novel TNF-NPY cross talk that modulates inflammation, barrier functions, and colonic motility during inflammation. It is also suggested that selective blocking of soluble TNF may be a better therapeutic option than using anti-TNF antibodies. Copyright © 2013 Crohn's & Colitis Foundation of America, Inc.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84888354417&origin=inward; http://dx.doi.org/10.1097/01.mib.0000437042.59208.9f; http://www.ncbi.nlm.nih.gov/pubmed/24108115; https://academic.oup.com/ibdjournal/article/19/12/2535-2546/4603009; https://dx.doi.org/10.1097/01.mib.0000437042.59208.9f; https://academic.oup.com/ibdjournal/article-abstract/19/12/2535/4603009?redirectedFrom=fulltext
Oxford University Press (OUP)
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