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The novel Listeria monocytogenes bile sensor BrtA controls expression of the cholic acid efflux pump MdrT.
Mol Microbiol. 2011 Jul; 81(1):129-42
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19 May 2011
New Finding
DOI: 10.3410/f.10576956.11439054
This is an interesting and fascinating report showing how pathogens (Listeria monocytogenes) can cope with the ‘harsh’ environmental conditions when entering the mammalian gastrointestinal system. It demonstrates that Listeria has a novel bile acid sensor that triggers cellular defense mechanisms when...Continue reading
This is an interesting and fascinating report showing how pathogens (Listeria monocytogenes) can cope with the ‘harsh’ environmental conditions when entering the mammalian gastrointestinal system. It demonstrates that Listeria has a novel bile acid sensor that triggers cellular defense mechanisms when bacteria are exposed to bile acids.
Bacteria -- whether pathogens or commensals -- that enter the human system via the oral route are exposed to a rather ‘harsh’ environment. Next to a low pH in stomach, bile acids in the intestinal lumen that can act as detergents are considered to potently inhibit bacterial growth. Amongst the defense systems that may have evolved to give an advantage of Listeria monocytogenes to survive in the gut, enter the host, and even undergo enterohepatic circulation, the present paper describes a fascinating mechanism. Listeria obviously expresses a novel bile acid receptor that controls, in the bacteria, the expression of ATP-driven efflux pumps that can export the bile acids and reduce their harmful effects on survival.
Bacteria -- whether pathogens or commensals -- that enter the human system via the oral route are exposed to a rather ‘harsh’ environment. Next to a low pH in stomach, bile acids in the intestinal lumen that can act as detergents are considered to potently inhibit bacterial growth. Amongst the defense systems that may have evolved to give an advantage of Listeria monocytogenes to survive in the gut, enter the host, and even undergo enterohepatic circulation, the present paper describes a fascinating mechanism. Listeria obviously expresses a novel bile acid receptor that controls, in the bacteria, the expression of ATP-driven efflux pumps that can export the bile acids and reduce their harmful effects on survival.
Disclosures
None declared
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Daniel H: F1000Prime Recommendation of [Quillin SJ et al., Mol Microbiol 2011, 81(1):129-42]. In F1000Prime, 19 May 2011; DOI: 10.3410/f.10576956.11439054. F1000Prime.com/10576956#eval11439054
F1000Prime Recommendations, Dissents and Comments for [Quillin SJ et al., Mol Microbiol 2011, 81(1):129-42]. In F1000Prime, 24 May 2013; F1000Prime.com/10576956
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Mammalian bile has potent anti-microbial activity, yet bacterial pathogens of the gastrointestinal tract and hepatobiliary system nonetheless persist and replicate within bile-rich environments. Listeria monocytogenes, a Gram-positive pathogen, encounters bile at three stages throughout its infectious cycle in vivo: in the gut during initial infection, in the liver where it replicates robustly and in the gallbladder, from which it can return to the intestine and thence to the environment. The mechanisms by which L. monocytogenes senses mammalian bile and counteracts its bactericidal effects are not fully understood. In this report, we have determined the L. monocytogenes bile-induced transcriptome, finding that many critical virulence factors are regulated by bile. Among these, the multidrug efflux pumps MdrM and MdrT, previously shown to be critical for the bacterial provocation of a pathogenesis-promoting host innate immune response, are robustly and specifically induced by the bile component cholic acid. This induction is mediated by BrtA, the first identified L. monocytogenes sensor of bile, which loses the ability to bind to and repress the mdrT promoter in the presence of cholic acid. We show that MdrT can export cholic acid, and that ΔmdrT bacteria are significantly attenuated both in vitro when exposed to cholic acid or bile, and in vivo in the gallbladders and livers of infected mice.
© 2011 Blackwell Publishing Ltd.
DOI: 10.1111/j.1365-2958.2011.07683.x
PMID: 21542862
