scholarly journals Cross Talk between SigB and PrfA in Listeria monocytogenes Facilitates Transitions between Extra- and Intracellular Environments

Author(s):  
Ahmed Gaballa ◽  
Veronica Guariglia-Oropeza ◽  
Martin Wiedmann ◽  
Kathryn J. Boor

SUMMARY The foodborne pathogen Listeria monocytogenes can modulate its transcriptome and proteome to ensure its survival during transmission through vastly differing environmental conditions. While L. monocytogenes utilizes a large array of regulators to achieve survival and growth in different intra- and extrahost environments, the alternative sigma factor σB and the transcriptional activator of virulence genes protein PrfA are two key transcriptional regulators essential for responding to environmental stress conditions and for host infection. Importantly, emerging evidence suggests that the shift from extrahost environments to the host gastrointestinal tract and, subsequently, to intracellular environments requires regulatory interplay between σB and PrfA at transcriptional, posttranscriptional, and protein activity levels. Here, we review the current evidence for cross talk and interplay between σB and PrfA and their respective regulons and highlight the plasticity of σB and PrfA cross talk and the role of this cross talk in facilitating successful transition of L. monocytogenes from diverse extrahost to diverse extra- and intracellular host environments.

2018 ◽  
Vol 7 (13) ◽  
Author(s):  
Yanhong Liu ◽  
Aixia Xu ◽  
Pina M. Fratamico ◽  
Christopher H. Sommers ◽  
Luca Rotundo ◽  
...  

Listeria monocytogenes is an important foodborne pathogen that causes listeriosis. Here, we report the draft genome sequences of seven L. monocytogenes strains isolated from food, environmental, and clinical sources.


2020 ◽  
Vol 86 (22) ◽  
Author(s):  
Tracey Lee Peters ◽  
Yaxiong Song ◽  
Daniel W. Bryan ◽  
Lauren K. Hudson ◽  
Thomas G. Denes

ABSTRACT Bacteriophages (phages) are currently available for use by the food industry to control the foodborne pathogen Listeria monocytogenes. Although phage biocontrols are effective under specific conditions, their use can select for phage-resistant bacteria that repopulate phage-treated environments. Here, we performed short-term coevolution experiments to investigate the impact of single phages and a two-phage cocktail on the regrowth of phage-resistant L. monocytogenes and the adaptation of the phages to overcome this resistance. We used whole-genome sequencing to identify mutations in the target host that confer phage resistance and in the phages that alter host range. We found that infections with Listeria phages LP-048, LP-125, or a combination of both select for different populations of phage-resistant L. monocytogenes bacteria with different regrowth times. Phages isolated from the end of the coevolution experiments were found to have gained the ability to infect phage-resistant mutants of L. monocytogenes and L. monocytogenes strains previously found to be broadly resistant to phage infection. Phages isolated from coinfected cultures were identified as recombinants of LP-048 and LP-125. Interestingly, recombination events occurred twice independently in a locus encoding two proteins putatively involved in DNA binding. We show that short-term coevolution of phages and their hosts can be utilized to obtain mutant and recombinant phages with adapted host ranges. These laboratory-evolved phages may be useful for limiting the emergence of phage resistance and for targeting strains that show general resistance to wild-type (WT) phages. IMPORTANCE Listeria monocytogenes is a life-threatening bacterial foodborne pathogen that can persist in food processing facilities for years. Phages can be used to control L. monocytogenes in food production, but phage-resistant bacterial subpopulations can regrow in phage-treated environments. Coevolution experiments were conducted on a Listeria phage-host system to provide insight into the genetic variation that emerges in both the phage and bacterial host under reciprocal selective pressure. As expected, mutations were identified in both phage and host, but additionally, recombination events were shown to have repeatedly occurred between closely related phages that coinfected L. monocytogenes. This study demonstrates that in vitro evolution of phages can be utilized to expand the host range and improve the long-term efficacy of phage-based control of L. monocytogenes. This approach may also be applied to other phage-host systems for applications in biocontrol, detection, and phage therapy.


2017 ◽  
Vol 5 (49) ◽  
Author(s):  
Taylor W. Bailey ◽  
Naila C. do Nascimento ◽  
Arun K. Bhunia

ABSTRACT Listeria monocytogenes is an opportunistic invasive foodborne pathogen. Here, we performed whole-genome sequencing of L. monocytogenes strain F4244 (serotype 4b) using Illumina sequencing. The sequence showed 94.5% identity with strain F2365, serotype 4b, and 90.6% with EGD-e, serotype 1/2a.


2011 ◽  
Vol 79 (9) ◽  
pp. 3596-3606 ◽  
Author(s):  
Chris S. Rae ◽  
Aimee Geissler ◽  
Paul C. Adamson ◽  
Daniel A. Portnoy

ABSTRACTListeria monocytogenesis a Gram-positive intracellular pathogen that is naturally resistant to lysozyme. Recently, it was shown that peptidoglycan modification by N-deacetylation or O-acetylation confers resistance to lysozyme in various Gram-positive bacteria, includingL. monocytogenes.L. monocytogenespeptidoglycan is deacetylated by the action ofN-acetylglucosamine deacetylase (Pgd) and acetylated byO-acetylmuramic acid transferase (Oat). We characterized Pgd−, Oat−, and double mutants to determine the specific role ofL. monocytogenespeptidoglycan acetylation in conferring lysozyme sensitivity during infection of macrophages and mice. Pgd−and Pgd−Oat−double mutants were attenuated approximately 2 and 3.5 logs, respectively,in vivo. In bone-marrow derived macrophages, the mutants demonstrated intracellular growth defects and increased induction of cytokine transcriptional responses that emanated from a phagosome and the cytosol. Lysozyme-sensitive mutants underwent bacteriolysis in the macrophage cytosol, resulting in AIM2-dependent pyroptosis. Each of thein vitrophenotypes was rescued upon infection of LysM−macrophages. The addition of extracellular lysozyme to LysM−macrophages restored cytokine induction, host cell death, andL. monocytogenesgrowth inhibition. This surprising observation suggests that extracellular lysozyme can access the macrophage cytosol and act on intracellular lysozyme-sensitive bacteria.


2016 ◽  
Vol 84 (6) ◽  
pp. 1806-1814 ◽  
Author(s):  
Diego E. Alvarez ◽  
Hervé Agaisse

Listeria monocytogenesis an intracellular pathogen that disseminates within the intestinal epithelium through acquisition of actin-based motility and formation of plasma membrane protrusions that project into adjacent cells. The resolution of membrane protrusions into vacuoles from which the pathogen escapes results in bacterial spread from cell to cell. This dissemination process relies on themlp-actA-plcBoperon, which encodes ActA, a bacterial nucleation-promoting factor that mediates actin-based motility, and PlcB, a phospholipase that mediates vacuole escape. Here we investigated the role of the metalloprotease Mpl in the dissemination process. In agreement with previous findings showing that Mpl is required for PlcB activation, infection of epithelial cells with the ΔplcBor Δmplstrains resulted in the formation of small infection foci. As expected, the ΔplcBstrain displayed a strong defect in vacuole escape. However, the Δmplstrain showed an unexpected defect in the resolution of protrusions into vacuoles, in addition to the expected but mild defect in vacuole escape. The Δmplstrain displayed increased levels of ActA on the bacterial surface in protrusions. We mapped an Mpl-dependent processing site in ActA between amino acid residues 207 to 238. Similar to the Δmplstrain, the ΔactA207–238strain displayed increased levels of ActA on the bacterial surface in protrusions. Although the ΔactA207–238strain displayed wild-type actin-based motility, it formed small infection foci and failed to resolve protrusions into vacuoles. We propose that, in addition to its role in PlcB processing and vacuole escape, the metalloprotease Mpl is required for ActA processing and protrusion resolution.


2015 ◽  
Vol 82 (3) ◽  
pp. 939-953 ◽  
Author(s):  
Jovana Kovacevic ◽  
Jennifer Ziegler ◽  
Ewa Wałecka-Zacharska ◽  
Aleisha Reimer ◽  
David D. Kitts ◽  
...  

ABSTRACTA novel genomic island (LGI1) was discovered inListeria monocytogenesisolates responsible for the deadliest listeriosis outbreak in Canada, in 2008. To investigate the functional role of LGI1, the outbreak strain 08-5578 was exposed to food chain-relevant stresses, and the expression of 16 LGI1 genes was measured. LGI1 genes with putative efflux (L. monocytogenesemrE[emrELm]), regulatory (lmo1851), and adhesion (sel1) functions were deleted, and the mutants were exposed to acid (HCl), cold (4°C), salt (10 to 20% NaCl), and quaternary ammonium-based sanitizers (QACs). Deletion oflmo1851had no effect on theL. monocytogenesstress response, and deletion ofsel1did not influence Caco-2 and HeLa cell adherence/invasion, whereas deletion ofemrEresulted in increased susceptibility to QACs (P< 0.05) but had no effect on the MICs of gentamicin, chloramphenicol, ciprofloxacin, erythromycin, tetracycline, acriflavine, and triclosan. In the presence of the QAC benzalkonium chloride (BAC; 5 μg/ml), 14/16 LGI1 genes were induced, andlmo1861(putative repressor gene) was constitutively expressed at 4°C, 37°C, and 52°C and in the presence of UV exposure (0 to 30 min). Following 1 h of exposure to BAC (10 μg/ml), upregulation ofemrE(49.6-fold),lmo1851(2.3-fold),lmo1861(82.4-fold), andsigB(4.1-fold) occurred. Reserpine visibly suppressed the growth of the ΔemrELmstrain, indicating that QAC tolerance is due at least partially to efflux activity. These data suggest that a minimal function of LGI1 is to increase the tolerance ofL. monocytogenesto QACs viaemrELm. Since QACs are commonly used in the food industry, there is a concern thatL. monocytogenesstrains possessingemrEwill have an increased ability to survive this stress and thus to persist in food processing environments.


2011 ◽  
Vol 80 (1) ◽  
pp. 100-109 ◽  
Author(s):  
Tania Véliz Rodriguez ◽  
Federica Moalli ◽  
Nadia Polentarutti ◽  
Moira Paroni ◽  
Eduardo Bonavita ◽  
...  

ABSTRACTToll interleukin-1 receptor (IL-1R) 8 (TIR8), also known as single Ig IL-1 receptor (IL-R)-related molecule, or SIGIRR, is a member of the IL-1R-like family, primarily expressed by epithelial cells. Current evidence suggests that TIR8 plays a nonredundant role as a negative regulatorin vivounder different inflammatory conditions that are dependent on IL-R and Toll-like receptor (TLR) activation. In the present study, we examined the role of TIR8 in innate resistance to acute lung infections caused byPseudomonas aeruginosa, a Gram-negative pathogen responsible for life-threatening infections in immunocompromised individuals and cystic fibrosis patients. We show that Tir8 deficiency in mice was associated with increased susceptibility to acuteP. aeruginosainfection, in terms of mortality and bacterial load, and to exacerbated local and systemic production of proinflammatory cytokines (gamma interferon [IFN-γ], tumor necrosis factor alpha [TNF-α], IL-1β, and IL-6) and chemokines (CXCL1, CXCL2, and CCL2). It has been reported that host defense againstP. aeruginosaacute lung infection can be improved by blocking IL-1 since exaggerated IL-1β production may be harmful for the host in this infection. In agreement with these data, IL-1RI deficiency rescues the phenotype observed in Tir8-deficient mice: in Tir8−/−IL-1RI−/−double knockout mice we observed higher survival rates, enhanced bacterial clearance, and reduced levels of local and systemic cytokine and chemokine levels than in Tir8-deficient mice. These results suggest that TIR8 has a nonredundant effect in modulating the inflammation caused byP. aeruginosa, in particular, by negatively regulating IL-1RI signaling, which plays a major role in the pathogenesis of this infectious disease.


2019 ◽  
Vol 8 (41) ◽  
Author(s):  
Lauren K. Hudson ◽  
Tracey L. Peters ◽  
Yaxiong Song ◽  
Thomas G. Denes

Bacteriophages that infect the foodborne pathogen Listeria monocytogenes were previously isolated from New York dairy farms. The complete genome sequences for three of these Listeria phages, with genome sizes of 64.6 to 65.7 kb, are presented here. Listeria phages LP-010, LP-013, and LP-031-2 are siphoviruses that belong to the genus Homburgvirus.


2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Lauren K. Hudson ◽  
Tracey Lee Peters ◽  
Daniel W. Bryan ◽  
Yaxiong Song ◽  
Henk C. den Bakker ◽  
...  

ABSTRACT Bacteriophages can be used as a biocontrol for the foodborne pathogen Listeria monocytogenes. Propagation of phages is a necessary step for their use in experimental studies and biocontrol applications. Here, we present the complete genomes of three Listeria monocytogenes strains commonly used as propagation hosts for Listeria phages.


2019 ◽  
Vol 8 (46) ◽  
Author(s):  
Tracey L. Peters ◽  
Lauren K. Hudson ◽  
Yaxiong Song ◽  
Thomas G. Denes

Bacteriophages isolated from environmental sources can be used as a biocontrol against the foodborne pathogen Listeria monocytogenes. Here, we present the complete genomes of LP-039 and LP-066, two Pecentumvirus bacteriophages that infect L. monocytogenes. The genome sizes of LP-039 and LP-066 are 136.2 kb and 139.0 kb, respectively.


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