摘要：Increase of the enteric bacteriophages (phage), components of the enteric virome, has been associated with the development of inflammatory bowel diseases. However, little is known about how a given phage contributes to the regulation of intestinal inflammation. In this study, we isolated a new phage associated with
Enterococcus gallinarum, named
phiEG37k, the level of which was increased in C57BL/6 mice with colitis development. We found that, irrespective of the state of inflammation, over 95% of the
E. gallinarum population in the mice contained
phiEG37k prophage within their genome and the
phiEG37k titers were proportional to that of
E. gallinarum in the gut. To explore whether
phiEG37k impacts intestinal homeostasis and/or inflammation, we generated mice colonized either with
E. gallinarum with or without the prophage
phiEG37k. We found that the mice colonized with the bacteria with
phiEG37k produced more Mucin 2 (MUC2) that serves to protect the intestinal epithelium, as compared to those colonized with the phage-free bacteria. Consistently, the former mice were less sensitive to experimental colitis than the latter mice. These results suggest that the newly isolated phage has the potential to protect the host by strengthening mucosal integrity. Our study may have clinical implication in further understanding of how bacteriophages contribute to the gut homeostasis and pathogenesis.
