scholarly journals Bacteriocin from epidemic Listeria strains alters the host intestinal microbiota to favor infection

2016 ◽  
Vol 113 (20) ◽  
pp. 5706-5711 ◽  
Author(s):  
Juan J. Quereda ◽  
Olivier Dussurget ◽  
Marie-Anne Nahori ◽  
Amine Ghozlane ◽  
Stevenn Volant ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Intestinal Microbiota ◽  
Virulence Factor ◽  
Invasive Disease ◽  
Immunocompromised Patients ◽  
Intestinal Colonization ◽  
Healthy Individuals ◽  
Virulence Potential ◽  
Evolutionary Lineages ◽  
Organ Infection

Listeria monocytogenes is responsible for gastroenteritis in healthy individuals and for a severe invasive disease in immunocompromised patients. Among the three identified L. monocytogenes evolutionary lineages, lineage I strains are overrepresented in epidemic listeriosis outbreaks, but the mechanisms underlying the higher virulence potential of strains of this lineage remain elusive. Here, we demonstrate that Listeriolysin S (LLS), a virulence factor only present in a subset of lineage I strains, is a bacteriocin highly expressed in the intestine of orally infected mice that alters the host intestinal microbiota and promotes intestinal colonization by L. monocytogenes, as well as deeper organ infection. To our knowledge, these results therefore identify LLS as the first bacteriocin described in L. monocytogenes and associate modulation of host microbiota by L. monocytogenes epidemic strains to increased virulence.

scholarly journals Bacteriocins of Listeria monocytogenes and Their Potential as a Virulence Factor

Toxins ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 103
Author(s):  
Sangmi Lee
Keyword(s):  
Listeria Monocytogenes ◽  
Virulence Factors ◽  
Intestinal Microbiota ◽  
Virulence Factor ◽  
Mode Of Action ◽  
Foodborne Pathogen ◽  
Protective Effects ◽  
Fatality Rate ◽  
Factors Affecting ◽  
High Fatality Rate

Intestinal microbiota exerts protective effects against the infection of various bacterial pathogens, including Listeria monocytogenes, a major foodborne pathogen whose infection can lead to a disease (listeriosis) with a high fatality rate. As a strategy to mitigate the action of the intestinal microbiota, pathogens often produce antimicrobial proteinaceous compounds such as bacteriocins. In this review, we summarize the information currently available for the well-characterized L. monocytogenes bacteriocin listeriolysin S, with the emphasis on its intriguing mode of action as a virulence factor, which promotes the infection of L. monocytogenes by changing the composition of the intestinal microbiota. We then discuss another intriguing L. monocytogenes bacteriocin Lmo2776 that specifically inhibits the inflammogenic species, Prevotella copri, in the intestinal microbiota, reducing superfluous inflammation while weakening virulence. In addition, we describe relatively less studied phage tail-like Listeria bacteriocins (monocins) and elaborate on the possibility that these monocins could be involved in enhancing pathogenicity. In spite of the burgeoning interest in the roles played by the intestinal microbiota against the L. monocytogenes infection, our understanding on the virulence factors affecting the intestinal microbiota is still lacking, calling for further studies on bacteriocins that could function as novel virulence factors.

scholarly journals Refinement of a Live Attenuated Salmonella enterica Serovar Newport Vaccine with Improved Safety

Vaccines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 57
Author(s):  
Shamima Nasrin ◽  
Fabien J. Fuche ◽  
Khandra T. Sears ◽  
Jennifer A. Jones ◽  
Myron M. Levine ◽  
...  
Keyword(s):  
Vaccine Efficacy ◽  
Invasive Disease ◽  
Immunocompromised Patients ◽  
Bacterial Burden ◽  
Igg Antibodies ◽  
Healthy Individuals ◽  
Wild Type ◽  
Lethal Challenge ◽  
Functional Antibodies

Non-typhoidal Salmonella (NTS) is a major cause of gastroenteritis and is responsible for approximately 93 million cases annually. In healthy individuals, gastroenteritis caused by NTS is usually self-limiting, however, NTS can cause severe invasive disease in immunocompromised patients. Very little research has been directed towards development of vaccines against Salmonella serogroups O:6,7 or O:8. We have constructed a live attenuated serogroup O:8 vaccine, CVD 1979, by deleting guaBA, htrA, and aroA from the genome of S. Newport. We have shown that the candidate vaccine is well tolerated in mice and elicits serum immunoglobulin G (IgG) antibodies against core O-polysaccharide (COPS) when administered orally. Immunized mice were challenged intraperitoneally with wild-type S. Newport and bacterial burden in the liver and spleen was found to be significantly reduced in the livers of immunized mice compared to control mice. We also observed moderate vaccine efficacy (45%) against lethal challenge with the serogroup O:8 serovar, S. Muenchen, but low vaccine efficacy (28%) following lethal challenge with a serogroup O:6,7 serovar, S. Virchow. In vitro, we have shown that antibodies generated by CVD 1979 only recognize lipopolysaccharide (LPS) from serogroup O:8 but not serogroup O:6,7 serovars, and that they mediate opsonophagocytic antibody (OPA) activity against serogroup O:8 but not serogroup O:6,7 serovars. We also showed that OPA activity can be blocked by pre-incubating the antisera with serogroup O:8 lipopolysaccharide. Taken together, our data demonstrate that we have constructed a well-tolerated, effective live attenuated S. Newport vaccine which elicits functional antibodies against serogroup O:8 but not O:6,7 serovars.

scholarly journals Listerial Rhombencephalitis in an Immunocompetent Woman

2014 ◽  
Vol 2014 ◽  
pp. 1-4
Author(s):  
Piotr Czupryna ◽  
Agata Zajkowska ◽  
Adam Garkowski ◽  
Sławomir Pancewicz ◽  
Katarzyna Guziejko ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Clinical Picture ◽  
Viral Encephalitis ◽  
Severe Form ◽  
Immunocompromised Patients ◽  
Healthy Individuals ◽  
Laboratory Results ◽  
History Of ◽  
Proper Diagnosis ◽  
Immunocompetent Patients

Listeriosis usually affects immunocompromised patients including elderly people and pregnant women, but it may also affect otherwise healthy individuals. In our report, we present a case of a rare and very severe form of listeriosis-rhombencephalitis in a 61-year-old female with no history of immunosuppression, who, because of history, clinical picture, and laboratory results as well as negative cultures, was at first diagnosed with viral encephalitis. This paper underlines thatListeria monocytogenesinfection should be taken into consideration in case of lymphocytic encephalitis even in immunocompetent patients. Typical MRI picture may be crucial in establishing a proper diagnosis as the lab results may be misleading.

scholarly journals MetR-Regulated Vibrio cholerae Metabolism Is Required for Virulence

mBio ◽  
2012 ◽  
Vol 3 (5) ◽  
Author(s):  
Ryan W. Bogard ◽  
Bryan W. Davies ◽  
John J. Mekalanos
Keyword(s):  
Amino Acid ◽  
Vibrio Cholerae ◽  
Virulence Factor ◽  
Current Knowledge ◽  
Intestinal Colonization ◽  
Wild Type ◽  
Pathogenic Potential ◽  
Content Type ◽  
Mouse Intestine

ABSTRACTLysR-type transcriptional regulators (LTTRs) are the largest, most diverse family of prokaryotic transcription factors, with regulatory roles spanning metabolism, cell growth and division, and pathogenesis. Using a sequence-defined transposon mutant library, we screened a panel ofV. choleraeEl Tor mutants to identify LTTRs required for host intestinal colonization. Surprisingly, out of 38 LTTRs, only one severely affected intestinal colonization in the suckling mouse model of cholera: the methionine metabolism regulator, MetR. Genetic analysis of genes influenced by MetR revealed thatglyA1andmetJwere also required for intestinal colonization. Chromatin immunoprecipitation of MetR and quantitative reverse transcription-PCR (qRT-PCR) confirmed interaction with and regulation ofglyA1, indicating that misregulation ofglyA1is likely responsible for the colonization defect observed in themetRmutant. TheglyA1mutant was auxotrophic for glycine but exhibited wild-type trimethoprim sensitivity, making folate deficiency an unlikely cause of its colonization defect. MetJ regulatory mutants are not auxotrophic but are likely altered in the regulation of amino acid-biosynthetic pathways, including those for methionine, glycine, and serine, and this misregulation likely explains its colonization defect. However, mutants defective in methionine, serine, and cysteine biosynthesis exhibited wild-type virulence, suggesting that these amino acids can be scavenged in vivo. Taken together, our results suggest that glycine biosynthesis may be required to alleviate an in vivo nutritional restriction in the mouse intestine; however, additional roles for glycine may exist. Irrespective of the precise nature of this requirement, this study illustrates the importance of pathogen metabolism, and the regulation thereof, as a virulence factor.IMPORTANCEVibrio choleraecontinues to be a severe cause of morbidity and mortality in developing countries. Identification ofV. choleraefactors critical to disease progression offers the potential to develop or improve upon therapeutics and prevention strategies. To increase the efficiency of virulence factor discovery, we employed a regulator-centric approach to multiplex our in vivo screening capabilities and allow whole regulons inV. choleraeto be interrogated for pathogenic potential. We identified MetR as a new virulence regulator and serine hydroxymethyltransferase GlyA1 as a new MetR-regulated virulence factor, both required byV. choleraeto colonize the infant mouse intestine. Bacterial metabolism is a prerequisite to virulence, and current knowledge of in vivo metabolism of pathogens is limited. Here, we expand the known role of amino acid metabolism and regulation in virulence and offer new insights into the in vivo metabolic requirements ofV. choleraewithin the mouse intestine.

scholarly journals Characterisation of Listeria monocytogenes food-associated isolates to assess environmental fitness and virulence potential

2021 ◽  
pp. 109247
Author(s):  
Jessica A. Gray ◽  
P. Scott Chandry ◽  
Mandeep Kaur ◽  
Chawalit Kocharunchitt ◽  
John P. Bowman ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Virulence Potential ◽  
Environmental Fitness

scholarly journals Detection and Potential Virulence of Viable but Non-Culturable (VBNC) Listeria monocytogenes: A Review

2021 ◽  
Vol 9 (1) ◽  
pp. 194
Author(s):  
Nathan E. Wideman ◽  
James D. Oliver ◽  
Philip Glen Crandall ◽  
Nathan A. Jarvis
Keyword(s):  
Public Health ◽  
Listeria Monocytogenes ◽  
Viable Count ◽  
Vbnc State ◽  
Testing Methods ◽  
Tetrazolium Chloride ◽  
Definitive Evidence ◽  
Virulence Potential ◽  
Vbnc Bacteria ◽  
The Impact

The detection, enumeration, and virulence potential of viable but non-culturable (VBNC) pathogens continues to be a topic of discussion. While there is a lack of definitive evidence that VBNC Listeria monocytogenes (Lm) pose a public health risk, recent studies suggest that Lm in its VBNC state remains virulent. VBNC bacteria cannot be enumerated by traditional plating methods, so the results from routine Lm testing may not demonstrate a sample’s true hazard to public health. We suggest that supplementing routine Lm testing methods with methods designed to enumerate VBNC cells may more accurately represent the true level of risk. This review summarizes five methods for enumerating VNBC Lm: Live/Dead BacLightTM staining, ethidium monoazide and propidium monoazide-stained real-time polymerase chain reaction (EMA- and PMA-PCR), direct viable count (DVC), 5-cyano-2,3-ditolyl tetrazolium chloride-4′,6-diamidino-2-phenylindole (CTC-DAPI) double staining, and carboxy-fluorescein diacetate (CDFA) staining. Of these five supplementary methods, the Live/Dead BacLightTM staining and CFDA-DVC staining currently appear to be the most accurate for VBNC Lm enumeration. In addition, the impact of the VBNC state on the virulence of Lm is reviewed. Widespread use of these supplemental methods would provide supporting data to identify the conditions under which Lm can revert from its VBNC state into an actively multiplying state and help identify the environmental triggers that can cause Lm to become virulent. Highlights: Rationale for testing for all viable Listeria (Lm) is presented. Routine environmental sampling and plating methods may miss viable Lm cells. An overview and comparison of available VBNC testing methods is given. There is a need for resuscitation techniques to recover Lm from VBNC. A review of testing results for post VBNC virulence is compared

scholarly journals Fatty Acids Regulate Stress Resistance and Virulence Factor Production for Listeria monocytogenes

2012 ◽  
Vol 194 (19) ◽  
pp. 5274-5284 ◽  
Author(s):  
Y. Sun ◽  
B. J. Wilkinson ◽  
T. J. Standiford ◽  
H. T. Akinbi ◽  
M. X. D. O'Riordan
Keyword(s):  
Fatty Acids ◽  
Listeria Monocytogenes ◽  
Virulence Factor ◽  
Stress Resistance ◽  
Factor Production ◽  
Virulence Factor Production

scholarly journals The inlA Gene of Listeria monocytogenesLO28 Harbors a Nonsense Mutation Resulting in Release of Internalin

1998 ◽  
Vol 66 (7) ◽  
pp. 3420-3422 ◽  
Author(s):  
Renaud Jonquières ◽  
Hélène Bierne ◽  
Jérôme Mengaud ◽  
Pascale Cossart
Keyword(s):  
Cell Adhesion ◽  
Listeria Monocytogenes ◽  
Virulence Factor ◽  
Adhesion Molecule ◽  
Nonsense Mutation ◽  
Cell Adhesion Molecule ◽  
Culture Medium ◽  
Surface Protein ◽  
Truncated Protein

ABSTRACT Internalin is a surface protein that mediates entry ofListeria monocytogenes EGD into epithelial cells expressing the cell adhesion molecule human E-cadherin or its chicken homolog, L-CAM, which act as receptors for internalin. After observing that entry of L. monocytogenes LO28 into S180 fibroblasts, in contrast to that of EGD, did not increase after transfection with L-CAM, we examined both the expression and the structure of internalin in strain LO28. We discovered a nonsense mutation in inlA which results in a truncated protein released in the culture medium. Mutations leading to release of internalin were also detected in clinical and food isolates. These results question the role of internalin as a virulence factor in murine listeriosis.

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