ORIGINAL RESEARCH article
Front. Microbiol.
Sec. Infectious Agents and Disease
This article is part of the Research TopicGut Microbiome's Role in Infectious Disease: Modulating Pathogens and Host ResponsesView all 4 articles
Lactobacillus paracasei LP18 ameliorated inflammation and intestinal barrier dysfunction in severe acute pancreatitis via gut microbiota–mediated regulation of butyrate metabolism
Provisionally accepted
- The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
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Severe acute pancreatitis (SAP) is closely associated with intestinal barrier disruption, bacterial translocation, and systemic inflammation. Increasing evidence suggests that disturbances in gut microbial metabolites, particularly short-chain fatty acids (SCFAs), contribute to epithelial injury, yet the mechanistic links remain insufficiently defined. This study investigated whether Lactobacillus paracasei LP18 alleviates SAP-induced intestinal barrier dysfunction by modulating gut metabolism, enhancing butyrate production, and suppressing NF-κB activation. SAP mice exhibited marked epithelial injury, villus atrophy, tight junction loss, elevated proinflammatory cytokines, and strong NF-κB activation. Untargeted metabolomics revealed extensive metabolic disruption, with significant alterations in butanoate metabolism and lipid-related pathways. LP18 administration reversed these abnormalities, restoring a metabolomic signature enriched in mucosa-protective metabolites. Targeted SCFA quantification showed profound butyrate depletion in SAP mice, whereas LP18 significantly increased butyrate levels and partially normalized acetate and propionate. Higher butyrate concentrations correlated with improved tight junction integrity and reduced oxidative stress. Mechanistically, LP18 inhibited phosphorylation and nuclear translocation of NF-κB p65, indicating effective suppression of inflammatory signaling. These anti-inflammatory effects were partially mediated by restored butyrate biosynthesis. Collectively, LP18 mitigates SAP-associated intestinal barrier injury by reprogramming gut metabolic profiles, enhancing endogenous butyrate production, and inhibiting NF-κB activation. These findings highlight LP18 as a promising microbiota-based therapeutic strategy for SAP-induced enteropathy and underscore the central role of microbial metabolites, especially butyrate, in linking metabolic disturbances to epithelial damage.
Keywords: butyratemetabolism, Gut Microbiota, Intestinal barrier dysfunction, Lactobacillus paracasei LP18, Severe acute pancreatitis
Received: 11 Dec 2025; Accepted: 26 Jan 2026.
Copyright: © 2026 Cao, Song, Zhang, Zhang, Jia, Li, Lan and Hu. 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: Yuepeng Hu
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