# Attenuation of Clostridioides difficile Infection by Clostridium hylemonae

## TL;DR

This study explores how Clostridium hylemonae may help reduce Clostridioides difficile infection by enhancing gut microbial diversity.

## Contribution

The study identifies Clostridium hylemonae as a potential probiotic with a novel mechanism of action against CDI.

## Key findings

- C. hylemonae DSM 15053 increased gut microbial diversity and richness in a CDI mouse model.
- The genera Phocaeicola, Akkermansia, and Parabacteroides were more abundant in C. hylemonae-treated mice.
- C. hylemonae mitigates CDI through a mechanism distinct from bile acid metabolism regulation.

## Abstract

Clostridioides difficile infection (CDI) is a bacterial infection of the colon that can cause diarrhea and colitis. The use of antimicrobials disrupts the intestinal microbiota, weakening colonization resistance and creating an environment in which C. difficile can establish infection. It is, therefore, necessary to identify specific bacteria that are helpful for the recovery of the intestinal microbiota in individuals with CDI. Previous studies have identified several strains that showed a negative correlation with C. difficile. Among these strains, C. hylemonae DSM 15053, which possesses the bai operon similar to Clostridium scindens, was selected. To test this hypothesis, we utilized a CDI mouse model and evaluated the inhibitory effect of C. hylemonae DSM 15053. Furthermore, to gain insights into the underlying mechanisms, we performed gut microbiota analysis. Contrary to our expectations, C. hylemonae DSM 15053 did not significantly produce SBAs. Interestingly, however, microbial diversity and richness were significantly higher in the C. hylemonae DSM 15053–treated group compared with the PBS control group. In addition, we observed a higher abundance of the genera Phocaeicola, Akkermansia, and Parabacteroides in the C. hylemonae DSM 15053 group. Moreover, metagenomic and metabolomic analyses revealed that C. hylemonae DSM 15053 mitigates CDI through a mechanism distinct from that of C. scindens KCTC 5591, which primarily functions as a regulator of bile acid metabolism.