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Characterization of Lactobacillus salivarius CECT 5713, a strain isolated from human milk: from genotype to phenotype.

Authors
  • Langa, Susana
  • Maldonado-Barragán, Antonio
  • Delgado, Susana
  • Martín, Rebeca
  • Martín, Virginia
  • Jiménez, Esther
  • Ruíz-Barba, José L
  • Mayo, Baltasar
  • Connor, Ruth I
  • Suárez, Juan Evaristo
  • Rodríguez, Juan M
Type
Published Article
Journal
Applied Microbiology and Biotechnology
Publisher
Springer-Verlag
Publication Date
Jun 01, 2012
Volume
94
Issue
5
Pages
1279–1287
Identifiers
DOI: 10.1007/s00253-012-4032-1
PMID: 22526789
Source
Medline
License
Unknown

Abstract

Lactobacillus salivarius CECT 5713, isolated from human milk, has immunomodulatory, anti-inflammatory and antiinfectious properties, as revealed by several in vitro and in vivo assays, which suggests a strong potential as a probiotic strain. In this work, the relationships between several genetic features of L. salivarius CECT 5713 and the corresponding phenotypes were evaluated. Although it contains a plasmid-encoded bacteriocin cluster, no bacteriocin biosynthesis was observed, possibly due to a 4-bp deletion at the beginning of the histidine kinase determinant abpK. The genome of L. salivarius CECT 5713 harbours two apparently complete prophages of 39.6 and 48 kbp. Upon induction, the 48-kbp prophage became liberated from the bacterial genome, but no DNA replication took place, which resulted in lysis of the cultures but not in phage progeny generation. The strain was sensitive to most antibiotics tested and no transmissible genes potentially involved in antibiotic resistance were detected. Finally, the genome of L. salivarius CECT 5713 contained four ORFs potentially involved in human molecular mimetism. Among them, protein 1230 was considered of particular relevance because of its similarity with dendritic cell-related proteins. Subsequently, in vitro assays revealed the ability of L. salivarius CECT 5713 to stimulate the maturation of immature dendritic cells and to inhibit the in vitro infectivity of HIV-1.

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