
94% of researchers rate our articles as excellent or good
Learn more about the work of our research integrity team to safeguard the quality of each article we publish.
Find out more
ORIGINAL RESEARCH article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1558845
This article is part of the Research TopicBiomarkers and Beyond: Predicting Course and Tailoring Treatment in Inflammatory Bowel DiseasesView all articles
The final, formatted version of the article will be published soon.
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Inflammatory bowel disease (IBD) is a complex immune-mediated condition, and biologics are the most commonly utilized pharmacological agents for its management. However, instances of treatment ineffectiveness persist. B-cell lymphoma 6 (Bcl6), a transcriptional repressor, is recognized for its regulatory effects on various immune-associated cell subsets. FX1, a novel specific inhibitor of BCL6's Bric-à-brac (BTB) domain, has demonstrated beneficial effects in numerous disease models; however, its impact and mechanisms in the context of IBD remain poorly understood. Therefore, we investigated the role of Bcl6 inhibition in a mouse model of DSS-induced colitis. Our data indicated that Disease Activity Index (DAI) scores were significantly reduced in the treatment group, with marked improvement observed in colitis symptoms. Additionally, there was a decrease in the proportion of macrophages within the colorectal environment and preservation of intestinal epithelial mucosal integrity. In vitro experiments revealed that following co-culture with macrophages, the Bcl6 inhibitor diminished pro-inflammatory factor secretion while enhancing expression levels of tight junction proteins in Caco2 cells.In conclusion, our experimental findings suggest that administration of the Bcl6 inhibitor can suppress inflammatory factor secretion by macrophages in murine models of colitis and safeguard intestinal barrier function. Thus, targeting BCL6 may represent a promising therapeutic strategy for managing IBD.
Keywords: BCL6, IBD, Pro-inflammatory cytokines, macrophage, tight junction proteins (TJPs)
Received: 11 Jan 2025; Accepted: 14 Apr 2025.
Copyright: © 2025 Liu, Zhang, Chuan, Wang, Zhang, Sun, Yao, Zhang, He, Yu, Xia, Liu, Ning and Feng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Zhe Zhang, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Baisui Feng, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
Supplementary Material
Research integrity at Frontiers
Learn more about the work of our research integrity team to safeguard the quality of each article we publish.