Bacteroides fragilis decrease intestinal Enterobacteriacease colonization and reverse metronidazole-induced bacterial translocation (120.22)

Abstract

Abstract Bacteroides, one of the major bacterial groups in the intestine, maintain a complex relationship with the host. In this study, the role of B. fragilis in intestinal permeability and immunity were examined in C57BL/6 mice receiving oral treatment of metronidazole for 6 days. Metronidazole treatment significantly decreased the number of B. fragilis but increased that of Enterobacteriaceae in intestinal mucosa and lumen. Metronidazole treatment increased intestinal permeability and pathogenic Klebsiella pneumoniae translocation. However, metronidazole did not change the bacterial killing activity and expression of TLR4, TLR2, MyD88, RegIIIβ, RegIIIγ, CRP-ductin, RELMβ, as well as defensin proteins in intestinal mucosa. Supplementation of dead B. fragilis in drinking water reversed the effects of metronidazole on intestinal permeability, Enterobacteriaceae colonization, and bacterial translocation (BT), suggesting that B. fragilis maintains intestinal permeability and decreases BT through reducing the colonization of Enterobacteriaceae rather than enhancing the expression of antibacterial proteins or the bacterial killing activity. This is further supported by that B. fragilis monoassociated mice showed a decrease of K. pneumoniae translocation and no change in bacterial killing activity as well as expression of defensin and nondefensin protein expression except of CRP-ductin when compared with germ free mice.