Abstract
An intestinal epithelium model able to produce mucus was developed to provide an environment suitable for testing the therapeutic activity of gut bacteriophages. We show that Enterococcus faecalis adheres more effectively in the presence of mucus, can invade the intestinal epithelia and is able to translocate after damaging tight junctions. Furthermore, Enterococcus phage vB_EfaM_A2 (a member of Herelleviridae that possesses virion associated immunoglobin domains) was found to translocate through the epithelium in the presence and absence of its host bacteria. Phage A2 protected eukaryotic cells by reducing mortality and maintaining the structure of the cell layer structure. We suggest the mammalian cell model utilized within this study as an adaptable in vitro model that can be employed to enable a better understanding of phage–bacteria interactions and the protective impact of phage therapy relating to the intestinal epithelium.
Highlights
Inflammatory bowel disease (IBD) includes both ulcerative colitis (UC) and Crohn’s disease (CD) and affects an estimated two million people in Europe [1]
The bacterial host used for its isolation was E. faecalis strain OG1RF, a human isolate that has been described to induce intestinal inflammation in mouse models of experimental colitis [13,50]
We describe the interaction of phage A2 and its host bacterium E. faecalis with respect to a mucus producing intestinal epithelial layer, better mimicking the conditions found in the mucosal layer of the human gut [49]
Summary
Inflammatory bowel disease (IBD) includes both ulcerative colitis (UC) and Crohn’s disease (CD) and affects an estimated two million people in Europe [1] It is a chronic inflammatory disorder with no single known cause, it is has been suggested to result from intestinal bacteria inducing an unwarranted activation of the gut’s mucosal immune system [2]. Most of the treatments developed for IBD use small molecules, vaccines, anti-TNF, or monoclonal antibodies to modulate the immune response in the gut [4,5,6] These therapies fail for a third of patients, most likely because of the complexity of the disease and the suggested imbalance of the gut microbiota [7,8,9]. Targetting and reducing levels of such bacterial strains like E. faecalis could potentially help to alleviate IBD symptoms
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