ORIGINAL RESEARCH article
Front. Microbiol.
Sec. Food Microbiology
Volume 16 - 2025 | doi: 10.3389/fmicb.2025.1560441
This article is part of the Research TopicProbiotics for Global Health: Advances, Applications and ChallengesView all 28 articles
The mitigative effects of Blautia producta 1009924 on intestinal inflammation induced by DSS
Provisionally accepted- 1Guangdong Medical University, Zhanjiang, Guangdong, China
- 2Guangdong Longseek Testing Co., Ltd., Guangzhou,Guangdong, China
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
Recent studies have indicated an association between the abundance of Blautia producta and inflammatory bowel disease (IBD) in hosts. In this study, the strain Blautia producta 1009924 (B. producta 1009924) was isolated from fresh fecal samples, and its biological characteristics and genomic features were analyzed. This strain is a strict anaerobe, forming circular, off-white colonies on BHI medium. It is Gram-positive, arranged in chains, and field emission scanning electron microscopy revealed abundant surface folds and pilus structures, along with excellent acid and bile salt tolerance. Whole-genome sequencing showed a total gene length of 6.05 Mb, a GC content of 45.72 %, and 5,214 coding genes with no virulence genes. KEGG database annotation indicated that its gene functions are mainly enriched in metabolic pathways, environmental information processing, and genetic information processing, with abundant gene clusters involved in lipid metabolism and short-chain fatty acid (SCFA) metabolic pathways.To investigate its role in alleviating intestinal inflammation, a zebrafish intestinal inflammation model induced by 0.5 % DSS for 72 hours was used for evaluation. Results showed that compared with the DSS-induced enteritis model group, B. producta 1009924 inhibited reactive oxygen species (ROS) production and neutrophil accumulation in zebrafish intestines. Histopathological analysis confirmed that it alleviated DSS-induced intestinal tissue damage, such as increasing goblet cell numbers and improving intestinal villus architecture. Real-time quantitative polymerase chain reaction (RT-qPCR) analysis demonstrated that B. producta 1009924 suppressed the activation of the TLR4/NF-κB signaling pathway by downregulating the expression of TLR4, MyD88, and NF-κB genes, thereby reducing the expression of pro-inflammatory factors (IL-6, IL-12) and the immune factor IL-10.Additionally, metabolomic analysis revealed that B. producta 1009924 regulated intestinal metabolism by increasing SCFA levels, including butyric acid and isovaleric acid. In conclusion, Blautia producta 1009924 significantly alleviates DSS-induced intestinal inflammation in zebrafish by regulating ROS levels, inhibiting excessive immune and inflammatory responses, and improving SCFA metabolism, highlighting its potential as a candidate strain for IBD treatment.
Keywords: Blautia producta 1009924, Genome, intestinal inflammation, inflammatory and, Short-chain fatty acids (SCFAs)
Received: 14 Jan 2025; Accepted: 14 Jul 2025.
Copyright: © 2025 Chen, Ma, Leng, Li, Qin, Li, Zhang and Yu. 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: Huajun Yu, Guangdong Medical University, Zhanjiang, 524023, Guangdong, 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.