Lentinan Exerts its Anti-Inflammatory Activity by Suppressing TNFR1 Transfer to the Surface of Intestinal Epithelial Cells through Dectin-1 in an in vitro and mice model


Lentinan Exerts its Anti-Inflammatory Activity by Suppressing TNFR1 Transfer to the Surface of Intestinal Epithelial Cells through Dectin-1 in an in vitro and mice model

It has been reported that lentinan, β-1,3; 1,6-glucan derived from Lentinula edodes, suppresses intestinal inflammation and ameliorates symptoms of colitis. However, the mechanism of intestinal anti-inflammatory activity of lentinan and how it is recognized by intestinal epithelial cells remains largely unclear. The receptor for lentinan on intestinal epithelial cells was identified using an in vitro gut inflammation model consisting of Caco-2 and RAW264.7 cells. Colitis was induced in 7 to 8 week-old wild-type (WT) or knockout (KO) mice by the free intake of water containing 2% dextran sulfate sodium (DSS) for 7 days. Lentinan was administered daily via intragastric administration. Tumor necrosis factor receptor 1 (TNFR1)-GFP complex was constructed to monitor its movement in Caco-2 cells using confocal and total internal fluorescence microscopy. The results indicated that lentinan suppressed DSS-induced body weight loss, shortening of colon length, histological score, and inflammatory cytokine mRNA expression in the inflamed tissues of WT mice, whereas these suppressive effects of lentinan were not observed in Dectin-1 KO mice. Furthermore, lentinan reduced TNFR1 expression in intestinal epithelial cells of WT mice but not those from Dectin-1 KO mice. Using TNFR1-GFP constructs, it was confirmed that lentinan reduced TNFR1 expression on Caco-2 cell membranes through Dectin-1 ligation. Our study revealed that lentinan suppressed intestinal inflammation by Dectin-1-mediated regulation of TNFR1 transfer to the surface of intestinal epithelial cells.

To know more about the article: https://www.longdom.org/archive/imr-volume-14-issue-3-year-2018.html

A standard editorial manager system is utilized for manuscript submission, review, editorial processing and tracking which can be securely accessed by the authors, reviewers and editors for monitoring and tracking the article processing. Manuscripts can be uploaded online at Editorial Tracking System (https://www.longdom.org/submissions/immunome-research.html) or forwarded to the Editorial Office at: immunores@longdom.org

How we work:

  • After submission, an acknowledgement with manuscript number is sent to the corresponding author within 7 working days.
  • A 21 day window time frame is allotted for peer-review process wherein multiple experts are contacted.
  • Author proof is generated within 7 working days after the acceptance decision.

Benefits on Publication:

Open Access: Permanent free access to your article upon publication ensures extensive global reach and readership.

Easy Article Sharing: Our open access enables you to share your article directly with colleagues through email and on social media via a single link, permitting third party reuse with appropriate citation in addition to the retention of content copyright by the author.

Global Marketing: Through promotion in a targeted global email announcement or press release, your article will be seen by thousands of the top-most thought-leaders in your field.

Reprints: Distribute your work to colleagues and at conferences as we provide hard copy color reprints of your article on order.

Media Contact:
Stella M
Journal Manager
Immunome Research
Email: immunores@longdom.org