期刊
APPLIED AND ENVIRONMENTAL MICROBIOLOGY
卷 81, 期 14, 页码 4642-4650出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/AEM.00281-15
关键词
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资金
- NIH [R56 AI088518-01A1]
- NIH T32 Training Program in Infectious Diseases and Microbial Immunology [5 T32 AI 7025-33]
- National Institute of General Medical Sciences ([NIGMS]) [T32GM083864, T32GM008336]
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 to C. jejuni, we found that mice treated with ampicillin are colonized by C. jejuni, with recovery of Campylobacter from the colon, mesenteric lymph nodes, and spleen. Furthermore, there was a significant reduction in recovery of C. jejuni from ampicillin-treated mice inoculated with a C. jejuni virulence mutant (Delta flgL strain) compared to recovery of mice inoculated with the C. jejuni wildtype strain or the C. jejuni complemented isolate (Delta flgL/flgL). Comparative analysis of the microbiota from nontreated and ampicillin- treated CBA/J mice led to the identification of a lactic acid-fermenting isolate of Enterococcus faecalis that prevented C. jejuni growth in vitro and limited C. 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 permits C. jejuni colonization. These findings provide valuable insights for researchers using mice to investigate C. jejuni colonization factors, virulence determinants, or the mechanistic basis of probiotics.
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