Gut microbiota and colonization resistance against bacterial enteric infection
Research output: Contribution to journal › Review article › peer-review
Colleges, School and Institutes
- Experimental Bacteriology, Department of Medical Microbiology, Leiden University Medical Center, Leiden, Netherlands.
- University of Michigan
- Netherlands Donor Feces Bank, Leiden, Netherlands.
The gut microbiome is critical in providing resistance against colonization by exogenous microorganisms. The mechanisms via which the gut microbiota provide colonization resistance (CR) have not been fully elucidated, but they include secretion of antimicrobial products, nutrient competition, support of gut barrier integrity, and bacteriophage deployment. However, bacterial enteric infections are an important cause of disease globally, indicating that microbiota-mediated CR can be disturbed and become ineffective. Changes in microbiota composition, and potential subsequent disruption of CR, can be caused by various drugs, such as antibiotics, proton pump inhibitors, antidiabetics, and antipsychotics, thereby providing opportunities for exogenous pathogens to colonize the gut and ultimately cause infection. In addition, the most prevalent bacterial enteropathogens, including Clostridioides difficile, Salmonella enterica serovar Typhimurium, enterohemorrhagic Escherichia coli, Shigella flexneri, Campylobacter jejuni, Vibrio cholerae, Yersinia enterocolitica, and Listeria monocytogenes, can employ a wide array of mechanisms to overcome colonization resistance. This review aims to summarize current knowledge on how the gut microbiota can mediate colonization resistance against bacterial enteric infection and on how bacterial enteropathogens can overcome this resistance.
|Journal||Microbiology and Molecular Biology Reviews|
|Early online date||5 Jun 2019|
|Publication status||Published - 1 Sep 2019|
- bacterial enteric infection, bacteriocins, bacteriophages, bile acids, colonization resistance, enteric pathogens, gut microbiota, microbiome, mucus layer, nutrient competition, short-chain fatty acids