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Peer-reviewedCC BY-NC 4.0Gut Microbes

Pathobiont-directed mucosal immunotherapy targets Ruminococcus gnavus and remodels host-microbiota interactions in colitis

  • Zhaoyi Wang1,2
  • Linlin Huang1
  • Xiaoxia Liu2
  • Xin Cheng2
  • Yuting Liang1,2
  • Jiayue Chen2
  • Ruihan Ma2
  • Wengang Song1
  • Xin Li1,2
  1. 1Department of Gastroenterology, Shandong Provincial Lab for Clinical Immunology Translational Medicine in Universities, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong, P. R. China
  2. 2Department of Medical Immunology, School of Clinical and Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China
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Abstract

Disease-associated pathobionts are recurrently enriched in inflammatory bowel disease (IBD), yet their causal contribution and selective therapeutic control remain incompletely defined. Here, through clinical microbiome profiling and causal animal studies, we identified Ruminococcus gnavus (Rg) as a key ulcerative colitis (UC)-associated pathobiont whose abundance positively correlates with intestinal oxidative stress and inflammatory levels. To selectively constrain Rg, we engineered CP-EV@Ca, an oral microbiota-directed mucosal immunotherapy that combines pathogen-specific immune targeting with redox modulation. CP-EV@Ca enhanced mucosal antigen presentation, promoted T follicular helper cell-germinal-center B-cell responses and induced robust Rg-specific secretory IgA (sIgA). CP-EV@Ca-induced mucosal immune responses, including enhanced Rg-specific sIgA production, were associated with increased immune coating and reduced Rg expansion. In both acute and chronic colitis models, CP-EV@Ca outperformed 5-aminosalicylic acid (5-ASA), suppressing inflammation and restoring microbial, epithelial and immune homeostasis. These findings demonstrate that pathobiont-specific mucosal immunity can be harnessed to selectively constrain disease-associated bacteria and restore intestinal homeostasis.

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Cite

BibTeXRIS
BibTeX
@article{wang2026pathobiontdirected,
  title = {{Pathobiont-directed mucosal immunotherapy targets Ruminococcus gnavus and remodels host-microbiota interactions in colitis}},
  author = {Zhaoyi Wang and Linlin Huang and Xiaoxia Liu and Xin Cheng and Yuting Liang and Jiayue Chen and Ruihan Ma and Wengang Song and Xin Li},
  journal = {Gut Microbes},
  year = {2026},
  month = oct,
  doi = {10.1080/19490976.2026.2754605},
  url = {https://doi.org/10.1080/19490976.2026.2754605},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Pathobiont-directed mucosal immunotherapy targets Ruminococcus gnavus and remodels host-microbiota interactions in colitis
AU  - Zhaoyi Wang
AU  - Linlin Huang
AU  - Xiaoxia Liu
AU  - Xin Cheng
AU  - Yuting Liang
AU  - Jiayue Chen
AU  - Ruihan Ma
AU  - Wengang Song
AU  - Xin Li
PY  - 2026
DA  - 2026/10/30
JO  - Gut Microbes
DO  - 10.1080/19490976.2026.2754605
UR  - https://doi.org/10.1080/19490976.2026.2754605
AB  - Disease-associated pathobionts are recurrently enriched in inflammatory bowel disease (IBD), yet their causal contribution and selective therapeutic control remain incompletely defined. Here, through clinical microbiome profiling and causal animal studies, we identified Ruminococcus gnavus (Rg) as a key ulcerative colitis (UC)-associated pathobiont whose abundance positively correlates with intestinal oxidative stress and inflammatory levels. To selectively constrain Rg, we engineered CP-EV@Ca, an oral microbiota-directed mucosal immunotherapy that combines pathogen-specific immune targeting with redox modulation. CP-EV@Ca enhanced mucosal antigen presentation, promoted T follicular helper cell-germinal-center B-cell responses and induced robust Rg-specific secretory IgA (sIgA). CP-EV@Ca-induced mucosal immune responses, including enhanced Rg-specific sIgA production, were associated with increased immune coating and reduced Rg expansion. In both acute and chronic colitis models, CP-EV@Ca outperformed 5-aminosalicylic acid (5-ASA), suppressing inflammation and restoring microbial, epithelial and immune homeostasis. These findings demonstrate that pathobiont-specific mucosal immunity can be harnessed to selectively constrain disease-associated bacteria and restore intestinal homeostasis.
SN  - 1949-0976
SN  - 1949-0984
ER  -