Bacterial communication in the regulation of stress response in Listeria monocytogenes

Twenty-nine strains of the foodborne pathogen Listeria monocytogenes were tested for their ability to colonize alfalfa, radish, and broccoli sprouts and their capacity to withstand acid and oxidative stress, two stresses common to the sprouting environment. Wide variation in the ability of different strains to colonize alfalfa sprouts were confirmed, but the variations among radish and broccoli sprouts were not as large. With a few exceptions, strains that were poor colonizers of alfalfa tended to be among the poorer colonizers of radish and broccoli and vice versa. The strains also were variable in their resistance to both acid and oxidative stress. Statistical analysis revealed no correlation between acid stress and sprout colonization, but there was a positive correlation between resistance to oxidative stress and colonization of all three sprout types. Although the response to oxidative stress is important for L. monocytogenes virulence, it also may be important for life outside of a host.

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Functional analysis of membrane vesicles of Listeria monocytogenes suggests a possible role in virulence and physiological stress response

Microbial Pathogenesis ◽

10.1016/j.micpath.2020.104076 ◽

2020 ◽

Vol 142 ◽

pp. 104076 ◽

Cited By ~ 2

Author(s):

Raman Karthikeyan ◽

Pratapa Gayathri ◽

Paramasamy Gunasekaran ◽

Medicharla V. Jagannadham ◽

Jeyaprakash Rajendhran

Keyword(s):

Functional Analysis ◽

Listeria Monocytogenes ◽

Stress Response ◽

Physiological Stress ◽

Membrane Vesicles ◽

Physiological Stress Response

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Transcriptional analysis of genes related to biofilm formation, stress-response, and virulence in Listeria monocytogenes strains grown at different temperatures

Annals of Microbiology ◽

10.1007/s13213-014-0814-2 ◽

2014 ◽

Vol 64 (4) ◽

pp. 1707-1714 ◽

Cited By ~ 4

Author(s):

Luiza Pieta ◽

Flavia Brusch Garcia ◽

Gustavo Pelicioli Riboldi ◽

Luisa Abruzzi de Oliveira ◽

Ana Paula Guedes Frazzon ◽

...

Keyword(s):

Listeria Monocytogenes ◽

Stress Response ◽

Biofilm Formation ◽

Transcriptional Analysis ◽

Different Temperatures

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Phenotypic and Transcriptomic Analyses Demonstrate Interactions between the Transcriptional Regulators CtsR and Sigma B in Listeria monocytogenes

Applied and Environmental Microbiology ◽

10.1128/aem.01085-07 ◽

2007 ◽

Vol 73 (24) ◽

pp. 7967-7980 ◽

Cited By ~ 42

Author(s):

Yuewei Hu ◽

Sarita Raengpradub ◽

Ute Schwab ◽

Chris Loss ◽

Renato H. Orsi ◽

...

Keyword(s):

Listeria Monocytogenes ◽

Stress Response ◽

Heat Resistance ◽

Parent Strain ◽

Inducible Promoter ◽

Heat Sensitivity ◽

Intestinal Epithelial ◽

Class Iii ◽

Stress Response Genes ◽

Genes Encoding

ABSTRACT Listeria monocytogenes σB positively regulates the transcription of class II stress response genes; CtsR negatively regulates class III stress response genes. To identify interactions between these two stress response systems, we constructed L. monocytogenes ΔctsR and ΔctsR ΔsigB strains, as well as a ΔctsR strain expressing ctsR in trans under the control of an IPTG (isopropyl-β-d-thiogalactopyranoside)-inducible promoter. These strains, along with a parent and a ΔsigB strain, were assayed for motility, heat resistance, and invasion of human intestinal epithelial cells, as well as by whole-genome transcriptomic and quantitative real-time PCR analyses. Both ΔctsR and ΔctsR ΔsigB strains had significantly higher thermotolerances than the parent strain; however, full heat sensitivity was restored to the ΔctsR strain when ctsR was expressed in trans. Although log-phase ΔctsR was not reduced in its ability to infect human intestinal cells, the ΔctsR ΔsigB strain showed significantly lower invasion efficiency than either the parent strain or the ΔsigB strain, indicating that interactions between CtsR and σB contribute to invasiveness. Statistical analyses also confirmed interactions between the ctsR and the sigB null mutations in both heat resistance and invasion phenotypes. Microarray transcriptomic analyses and promoter searches identified (i) 42 CtsR-repressed genes, (ii) 22 genes with lower transcript levels in the ΔctsR strain, and (iii) at least 40 genes coregulated by both CtsR and σB, including genes encoding proteins with confirmed or plausible roles in virulence and stress response. Our data demonstrate that interactions between CtsR and σB play an important role in L. monocytogenes stress resistance and virulence.

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Strand specific RNA-sequencing and membrane lipid profiling reveals growth phase-dependent cold stress response mechanisms in Listeria monocytogenes

PLoS ONE ◽

10.1371/journal.pone.0180123 ◽

2017 ◽

Vol 12 (6) ◽

pp. e0180123 ◽

Cited By ~ 14

Author(s):

Patricia Hingston ◽

Jessica Chen ◽

Kevin Allen ◽

Lisbeth Truelstrup Hansen ◽

Siyun Wang

Keyword(s):

Listeria Monocytogenes ◽

Stress Response ◽

Cold Stress ◽

Rna Sequencing ◽

Growth Phase ◽

Membrane Lipid ◽

Lipid Profiling

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Listeria monocytogenes Uses Listeria Adhesion Protein (LAP) To Promote Bacterial Transepithelial Translocation and Induces Expression of LAP Receptor Hsp60

Infection and Immunity ◽

10.1128/iai.00516-10 ◽

2010 ◽

Vol 78 (12) ◽

pp. 5062-5073 ◽

Cited By ~ 55

Author(s):

Kristin M. Burkholder ◽

Arun K. Bhunia

Keyword(s):

Plasma Membrane ◽

Listeria Monocytogenes ◽

Stress Response ◽

Cell Model ◽

Infection Process ◽

Intestinal Epithelial ◽

Necrosis Factor Alpha ◽

Adhesion Protein ◽

Hsp60 Expression

ABSTRACT Listeria monocytogenes interaction with the intestinal epithelium is a key step in the infection process. We demonstrated that Listeria adhesion protein (LAP) promotes adhesion to intestinal epithelial cells and facilitates extraintestinal dissemination in vivo. The LAP receptor is a stress response protein, Hsp60, but the precise role for the LAP-Hsp60 interaction during Listeria infection is unknown. Here we investigated the influence of physiological stressors and Listeria infection on host Hsp60 expression and LAP-mediated bacterial adhesion, invasion, and transepithelial translocation in an enterocyte-like Caco-2 cell model. Stressors such as heat (41°C), tumor necrosis factor alpha (TNF-α) (100 U), and L. monocytogenes infection (104 to 106 CFU/ml) significantly (P < 0.05) increased plasma membrane and intracellular Hsp60 levels in Caco-2 cells and consequently enhanced LAP-mediated L. monocytogenes adhesion but not invasion of Caco-2 cells. In transepithelial translocation experiments, the wild type (WT) exhibited 2.7-fold more translocation through Caco-2 monolayers than a lap mutant, suggesting that LAP is involved in transepithelial translocation, potentially via a paracellular route. Short hairpin RNA (shRNA) suppression of Hsp60 in Caco-2 cells reduced WT adhesion and translocation 4.5- and 3-fold, respectively, while adhesion remained unchanged for the lap mutant. Conversely, overexpression of Hsp60 in Caco-2 cells enhanced WT adhesion and transepithelial translocation, but not those of the lap mutant. Furthermore, initial infection with a low dosage (106 CFU/ml) of L. monocytogenes increased plasma membrane and intracellular expression of Hsp60 significantly, which rendered Caco-2 cells more susceptible to subsequent LAP-mediated adhesion and translocation. These data provide insight into the role of LAP as a virulence factor during intestinal epithelial infection and pose new questions regarding the dynamics between the host stress response and pathogen infection.

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