Phage: Future Treatment Direction for inflammatory bowel disease Patients
Inflammatory bowel disease (IBD) is characterized by tissue damage resulting from uncontrolled innate and acquired immune responses. It is an autoimmune disease, including ulcerative colitis (UC), Crohn's disease (CD) and indeterminate colitis (IC). The etiology of IBD is complex, and its clinical treatment faces significant challenges, necessitating urgent exploration of new treatment methods. Emerging evidence indicates that gut microbiota and IBD interact in the occurrence and development of diseases, emphasizing the importance of restoring gut microbiota imbalance. Phages have gained attention due to their potential to their potential to act on gut microbiota, offering advantages such as high efficiency, easy access, and ability to disrupt bacterial cell structures. Consequently, research into how phages interact with bacteria and their potential as a novel treatment for IBD has become a recent hotspot. Phages regulate intestinal inflammation by activating the immune system. Previous studies have observed an increase in the abundance of Caudovirales phages in IBD patients. Latest research reveals that special combinations of bacteriophages can effectively improve the symptoms of IBD model animals. This article reviews the interaction mechanism between phages and gut microbiota as well as the related research progress in IBD. The selection of articles retrieved on PubMed based on phage and Inflammatory bowel disease.
Authors
- Airu Liu
- Xiaotong Shen (ORCID: https://orcid.org/0000-0003-1300-1451)
- Xiaolan Zhang (ORCID: https://orcid.org/0000-0002-7047-3634)
- Xiaonan Liang (ORCID: https://orcid.org/0000-0002-6017-2184)
Institutions
- Hebei Medical University (CN)
- Second Hospital of Hebei Medical University (CN)
Publication Details
- Journal
- Microbiota & Diseases
- Published
- 2024-10-28
- DOI
- https://doi.org/10.54844/md.2023.0434
- Primary Topic
- Bacteriophages and microbial interactions
- Type
- article
- Field-Weighted Citation Impact
- 0.00