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A Putative Microcin Amplifies Shiga Toxin 2a Production of Escherichia coli O157:H7
Author(s) -
Hillary M. Mosso,
Lingzi Xiaoli,
Kakolie Banerjee,
Maria Hoffmann,
Kuan Yao,
Edward G. Dudley
Publication year - 2019
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.00353-19
Subject(s) - escherichia coli , biology , shiga toxin , prophage , microbiology and biotechnology , plasmid , toxin , enterobacteriaceae , bacteria , pathogen , bacteriocin , gene , shiga like toxin , operon , bacteriophage , genetics
How the gut microflora influences the progression of bacterial infections is only beginning to be understood. Antibiotics are counterindicated forE. coli O157:H7 infections, limiting treatment options. An increased understanding of how the gut microflora directs O157:H7 virulence gene expression may lead to additional treatment options. This work identifiedE. coli strains that enhance the production of Shiga toxin by O157:H7 through the secretion of a proposed microcin. Microcins are natural antimicrobial peptides that target specific species, can act as alternatives to antibiotics, and mediate microbial competition. This work demonstrates another mechanism by which non-O157E. coli strains may increase Shiga toxin production and adds to our understanding of microcins, a group of antimicrobials less well understood than colicins.

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