AniView Supports Intestinal Barrier Repair Research: Targeted intestinal barrier repair via probiotic-derived engineered outer membrane vesicles: A 3A1M strategy with antioxidant, anti-inflammatory

New progress has been made in targeted intestinal barrier repair using probiotic-derived engineered outer membrane vesicles.

Researcher Xiaojun Cai and Researcher Hui Deng from the Affiliated Stomatological Hospital of Wenzhou Medical University published their findings in “Acta Pharmaceutica Sinica B” (IF = 14.6, top journal).

This study developed a probiotic-derived engineered outer membrane vesicle platform that integrates antioxidant, anti-inflammatory, anti-ferroptotic, and microbiome-modulating functions, providing a safe, precise, and efficient therapeutic strategy for inflammatory bowel disease (IBD).

Inflammatory bowel disease (IBD) is a group of chronic, relapsing inflammatory disorders of the gastrointestinal tract, primarily including ulcerative colitis and Crohn's disease. Current therapeutic agents are limited by heterogeneous efficacy and significant side effects associated with long-term use. Therefore, there is an urgent need to develop novel and safe therapeutic strategies capable of regulating multiple pathological processes involved in IBD.

To address these challenges, the researchers developed GDO@CM. This formulation utilizes outer membrane vesicles (OMVs) derived from the probiotic Escherichia coli Nissle 1917 (EcN) as the delivery carrier. OMVs exhibit low immunogenicity, excellent biocompatibility, and an intrinsic ability to target intestinal epithelial and immune cells. Gallic acid (GA) and the hydrogen sulfide donor diallyl trisulfide (DATS) were co-encapsulated within the OMVs, while the surface was coated with macrophage membranes (CM) to enhance targeting to inflamed tissues. GA, a natural polyphenol, exerts potent antioxidant and anti-ferroptotic effects by scavenging reactive oxygen species (ROS), chelating metal ions, and enhancing antioxidant enzyme activity. DATS releases hydrogen sulfide in the presence of glutathione, activates the Nrf2/HO-1 signaling pathway, promotes the polarization of macrophages from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype, suppresses the production of pro-inflammatory cytokines, and facilitates intestinal barrier repair. By integrating the synergistic effects of natural polyphenols and gas therapy, this strategy offers a precise, safe, and highly effective therapeutic approach for IBD.

Experiments using Plantview

In this study, the researchers employed the AniView Multimodal In Vivo Imaging System developed by Guangzhou Biolight Biotechnology to evaluate the targeting capability and retention of GDO@CM.

A DSS-induced colitis mouse model was established by administering 3% DSS in drinking water for approximately seven days. Disease progression was evaluated by monitoring fecal blood and body weight changes. The mice were then randomly assigned to four treatment groups: PBS (DSS group), OMVs (OMVs group), GDO@CM (GDO@CM group), and 5-ASA (5-ASA group, used as the positive control). Healthy mice served as the normal control group. During the 11-day treatment period, all colitis model mice continued to receive 3% DSS in their drinking water to maintain intestinal inflammation. The OMVs, GDO@CM, and 5-ASA groups received rectal administration of the corresponding treatments on days 1, 3, 5, 7, and 9. In vivo imaging demonstrated that DiR-labeled GDO@CM (DiR-GDO@CM) was well retained in the colons of colitis mice 9 hours after rectal administration, indicating its excellent targeting and retention capabilities. In contrast, only a small amount of DiR-GDO@CM remained in the colons of healthy mice 6 hours after administration, further confirming the preferential retention of GDO@CM at sites of damaged colonic mucosa.

Therapeutic efficacy of GDO@CM in a DSS-induced colitis mouse model. (A) Schematic illustration of the experimental design. (B) Biodistribution of DiR-GDO@CM in the colon at different time points following rectal administration.

DOI: 10.1016/j.apsb.2026.01.031