Abstract
Bacteroides fragilis can be divided into two different groups of strains: an enterotoxigenic strain (ETBF) that has a pathogenicity island and the Bacteroides fragilis toxin gene (bft) and a non-toxigenic strain (NTBF) that does not have a pathogenicity island and the bft gene. Recent studies have shown that there is a correlation between the presence of the bft gene in enterotoxigenic Bacteroides fragilis (ETBF) strains and various gastrointestinal disorders, including colorectal cancer and inflammatory bowel disease. Due to its ability to disrupt the intestinal epithelial barrier, promote chronic inflammation, and affect carcinogenesis, the presence and expression of bft significantly contribute to the pathogenicity of ETBF. This review provides an analysis of the genetic structure, allelic variants, and regulatory mechanisms of bft. A membrane protein vital to cell adhesion, E-cadherin, is disrupted by Bacteroides fragilis toxin, resulting in disruption of epithelial integrity and facilitating bacterial entry. BFT also stimulates important intracellular signaling pathways, including mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light chain enhancer of activated B cells (NF-kB). These signaling pathways significantly influence both cellular transformation and inflammatory responses. This review also highlights advances in diagnostic methods and innovative therapeutic approaches, such as the development of allosteric inhibitors that can block BFT activity. Although much has been learned about the regulation and function of the bft gene, there are significant gaps in understanding the environmental factors that lead to gene upregulation and its molecular interactions. Future research should aim to elucidate these mechanisms to facilitate the development of targeted therapies.