The Intestinal Microbiota Influences Campylobacter jejuni Colonization and Extraintestinal Dissemination in Mice

Campylobacter jejuni is a leading cause of human foodborne gastroenteritis worldwide. The interactions between this pathogen and the intestinal microbiome within a host are of interest as endogenous intestinal microbiota mediates a form of resistance to the pathogen. This resistance, termed colonization resistance, is the ability of commensal microbiota to prevent colonization by exogenous pathogens or opportunistic commensals. Although mice normally demonstrate colonization resistance toC. jejuni , we found that mice treated with ampicillin are colonized byC. jejuni , with recovery ofCampylobacter from the colon, mesenteric lymph nodes, and spleen. Furthermore, there was a significant reduction in recovery ofC. jejuni from ampicillin-treated mice inoculated with aC. jejuni virulence mutant (ΔflgL strain) compared to recovery of mice inoculated with theC. jejuni wild-type strain or theC. jejuni complemented isolate (ΔflgL /flgL ). Comparative analysis of the microbiota from nontreated and ampicillin-treated CBA/J mice led to the identification of a lactic acid-fermenting isolate ofEnterococcus faecalis that preventedC. jejuni growthin vitro and limitedC. jejuni colonization of mice. Next-generation sequencing of DNA from fecal pellets that were collected from ampicillin-treated CBA/J mice revealed a significant decrease in diversity of operational taxonomic units (OTUs) compared to that in control (nontreated) mice. Taken together, we have demonstrated that treatment of mice with ampicillin alters the intestinal microbiota and permitsC. jejuni colonization. These findings provide valuable insights for researchers using mice to investigateC. jejuni colonization factors, virulence determinants, or the mechanistic basis of probiotics.