Affiliation:
1. Department of Microbiology and National Food Biotechnology Centre, University College Cork, Cork, Ireland
Abstract
ABSTRACT
Bile is one of many barriers that
Listeria monocytogenes
must overcome in the human gastrointestinal tract in order to infect and cause disease. We demonstrated that stationary-phase cultures of
L. monocytogenes
LO28 were able to tolerate concentrations of bovine, porcine, and human bile and bile acids well in excess of those encountered in vivo. Strain LO28 was relatively bile resistant compared with other clinical isolates of
L. monocytogenes
, as well as with
Listeria innocua
,
Salmonella enterica
serovar Typhimurium LT2, and
Lactobacillus sakei
. While exponential-phase
L. monocytogenes
LO28 cells were exquisitely sensitive to unconjugated bile acids, prior adaptation to sublethal levels of bile acids or heterologous stresses, such as acid, heat, salt, or sodium dodecyl sulfate (SDS), significantly enhanced bile resistance. This adaptive response was independent of protein synthesis, and in the cases of bile and SDS adaptation, occurred in seconds. In order to identify genetic loci involved in the bile tolerance phenotype of
L. monocytogenes
LO28, transposon (Tn
917
) and plasmid (pORI19) integration banks were screened for bile-sensitive mutants. The disrupted genes included a homologue of the
capA
locus required for capsule formation in
Bacillus anthracis
; a gene encoding the transcriptional regulator ZurR; a homologue of an
Escherichia coli
gene,
lytB
, involved in isoprenoid biosynthesis; a gene encoding a homologue of the
Bacillus subtilis
membrane protein YxiO; and a gene encoding an amino acid transporter with a putative role in pH homeostasis,
gadE
. Interestingly, all of the identified loci play putative roles in maintenance of the cell envelope or in stress responses.
Publisher
American Society for Microbiology
Subject
Ecology,Applied Microbiology and Biotechnology,Food Science,Biotechnology
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