期刊
PLOS ONE
卷 14, 期 7, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0220321
关键词
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资金
- National Research Foundation [102107]
- University of Pretoria
- U.S. Department of Agriculture National Institute of Food and Agriculture [1000028]
- USDA Agricultural Research Service [59-8072-6-001]
Background Listeria monocytogenes is an intracellular foodborne pathogen that employs a number of strategies to survive challenging gastrointestinal conditions. It proliferates in the gut and subsequently causes listeriosis in high-risk individuals. Therefore, inhibition of its adherence to the intestinal receptors is crucial in controlling its infection. In this study, the effect of our previously developed recombinant Lactobacillus casei strain expressing invasion protein, Internalin AB of L. monocytogenes (Lbc(InlAB)) on epithelial infection processes of the latter under simulated intestinal conditions was investigated. Materials and methods The confluent Caco-2 cell monolayer was pre-exposed to different L. casei strains at a multiplicity of exposure (MOE) of 10 for various periods before infection with L. monocytogenes at a multiplicity of infection (MOI) of 10 under simulated intestinal conditions. Subsequently, L. monocytogenes adhesion, invasion, and translocation, cytotoxicity and impact on tight junction integrity of the Caco-2 cells were analyzed. Results Under the simulated gastrointestinal condition, Lbc(InlAB) showed a significant increase (p<0.0001) in adherence to, invasion and translocation through the Caco-2 cells when compared with the wild type strain. Although Lbc(InlAB) strain exhibited enhanced inhibition of L. monocytogenes, it was not able to displace L. monocytogenes cells already attached to the monolayer. Additionally, pre-exposure to Lbc(InlAB) reduced L. monocytogenes-mediated cytotoxicity and protected the tight junction barrier function. Conclusion The recombinant L. casei expressing InlAB shows potential for use as a prophylactic intervention strategy for targeted control of L. monocytogenes during the intestinal phase of infection.
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