期刊
TRENDS IN FOOD SCIENCE & TECHNOLOGY
卷 127, 期 -, 页码 272-279出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tifs.2022.05.014
关键词
Lactic acid bacteria; AI-2; Quorum sensing; Biofilm formation; Gastrointestinal environment; Probiotics
资金
- National Natural Science Foundation of China [32072182, 32101910]
This review summarizes the different roles of AI-2 in lactic acid bacteria, including resistance to harsh environmental conditions, biofilm formation, adhesion and colonization, bacteriocin synthesis, and competition. AI-2 regulates communication among LAB and influences their probiotic activities. However, uncovering the AI-2 regulatory pathways in LAB remains a challenge.
Background: The LuxS/AI-2 quorum sensing system mediates interspecies and intraspecies signaling in bacteria and is associated with biofilm formation, pathogenicity, and resistance to harsh conditions. The regulatory mechanisms of the LuxS/AI-2 system in Vibrio harveyi, Escherichia coli, and Salmonella have been fully elucidated and have been termed lux operon and lsr operon. Furthermore, AI-2 is essential for the probiotic activities of lactic acid bacteria (LAB), including the gastrointestinal tract tolerance, adhesion, and colonization. However, there is limited information on the LuxS/AI-2 system in LAB.Scope and approach: The health benefits of LAB regulated by AI-2 are emerging as a new research area in the field of probiotics, although the number of reports is limited. In this review, the different aspects of AI-2, including AI2 synthesis and its roles in the resistance to harsh environmental conditions, biofilm formation, adhesion and colonization, bacteriocin synthesis, and competition in LAB, are summarized.Key findings and conclusions: AI-2 regulates the communication among LAB and their populations, thus influencing the probiotic activities of LAB. This review provides novel insights for the design of new, efficient, and specific probiotic products. However, the uncovering of the AI-2 regulatory pathways in LAB remains a critical challenge in the absence of AI-2 homologous proteins from of V. harveyi or E. coli.
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