If the more severe form of listeriosis develops, symptoms may include headache, stiff neck, confusion, loss of balance, and convulsions. For the very young, the elderly, and the immune-compromised listeriosis can result in death. People infected with L. More severe forms of listeriosis may take anywhere from three days to three months to develop. Due to the range in severity of illness, people should consult their health care provider if they suspect that they have developed symptoms that resemble a n L.
The severity of listeriosis varies and in some cases can be fatal, especially among the elderly, people with weakened immune systems or chronic diseases. Listeriosis can be particularly dangerous for pregnant women and their newborn babies, leading to serious complications with their pregnancy, including miscarriage and stillbirth.
Babies born with a listeriosis infection may develop severe health complications that require immediate medical attention, lead to lifelong health problems, or result in death. Traffic 13 , — Ribet, D. Listeria monocytogenes impairs SUMOylation for efficient infection. Impens, F. Promyelocytic leukemia protein PML controls Listeria monocytogenes infection. Boujemaa-Paterski, R.
Biochemistry 40 , — Jasnin, M. Three-dimensional architecture of actin filaments in Listeria monocytogenes comet tails. Truong, D. Bioessays 36 , — Fattouh, R. The diaphanous-related Formins promote protrusion formation and cell-to-cell spread of Listeria monocytogenes.
Rigano, L. Listeria monocytogenes antagonizes the human GTPase Cdc42 to promote bacterial spread. Rajabian, T. The bacterial virulence factor InlC perturbs apical cell junctions and promotes cell-to-cell spread of Listeria.
This work reveals that the L. Czuczman, M. Listeria monocytogenes exploits efferocytosis to promote cell-to-cell spread. This paper highlights the involvement of efferocytosis in the recipient cell during cell-to-cell spread. Auerbuch, V. Mice lacking the type I interferon receptor are resistant to Listeria monocytogenes. Carrero, J. Type I interferon sensitizes lymphocytes to apoptosis and reduces resistance to Listeria infection.
O'Connell, R. Type I interferon production enhances susceptibility to Listeria monocytogenes infection. Stockinger, S. Osborne, S. Type I interferon promotes cell-to-cell spread of Listeria monocytogenes. Gutierrez, M. Autophagy is a defense mechanism inhibiting BCG and Mycobacterium tuberculosis survival in infected macrophages.
Yoshikawa, Y. Listeria monocytogenes ActA-mediated escape from autophagic recognition. This paper identifies the importance of ActA-mediated autophagy evasion during L. Mostowy, S. Mitchell, G. Avoidance of autophagy mediated by PlcA or ActA is required for Listeria monocytogenes growth in macrophages.
Lecuit, M. A single amino acid in E-cadherin responsible for host specificity towards the human pathogen Listeria monocytogenes. EMBO J. A transgenic model for listeriosis: role of internalin in crossing the intestinal barrier. Pentecost, M. Listeria monocytogenes Internalin B activates junctional endocytosis to accelerate intestinal invasion. Gessain, G. PI3-kinase activation is critical for host barrier permissiveness to Listeria monocytogenes.
Khelef, N. Species specificity of the Listeria monocytogenes InlB protein. Wollert, T. Extending the host range of Listeria monocytogenes by rational protein design. Tsai, Y. Murinization of Internalin extends its receptor repertoire, altering Listeria monocytogenes cell tropism and host responses. Jones, G. Intracellular Listeria monocytogenes comprises a minimal but vital fraction of the intestinal burden following foodborne infection. Monocytes are the predominant cell type associated with Listeria monocytogenes in the gut, but they do not serve as an intracellular growth niche.
Bleriot, C. Liver-resident macrophage necroptosis orchestrates type 1 microbicidal inflammation and typemediated tissue repair during bacterial infection. Immunity 42 , — Charlier, C. Growth of Listeria monocytogenes in the guinea pig placenta and role of cell-to-cell spread in fetal infection.
Disson, O. Conjugated action of two species-specific invasion proteins for fetoplacental listeriosis. This study identifies key determinants required to cross the placental barrier.
Targeting and crossing of the human maternofetal barrier by Listeria monocytogenes : role of internalin interaction with trophoblast E-cadherin. Zeldovich, V. Invasive extravillous trophoblasts restrict intracellular growth and spread of Listeria monocytogenes. Placental syncytium forms a biophysical barrier against pathogen invasion. Faralla, C. InlP, a new virulence factor with strong placental tropism. Rolhion, N.
When pathogenic bacteria meet the intestinal microbiota. B Biol. Archambaud, C. Impact of lactobacilli on orally acquired listeriosis. The intestinal microbiota interferes with the microRNA response upon oral Listeria infection. Becattini, S. Commensal microbes provide first line defense against Listeria monocytogenes infection.
This study dissects the relative contributions of the microbiota and the immune response in listeriosis and identifies four strains of bacteria that have antibacterial properties against L.
Becavin, C. Cotter, P. Listeriolysin S, a novel peptide haemolysin associated with a subset of lineage I Listeria monocytogenes. Quereda, J. Bacteriocin from epidemic Listeria strains alters the host intestinal microbiota to favor infection.
This study identifies the first bacteriocin-like virulence factor in L. Listeria monocytogenes bile salt hydrolase is a PrfA-regulated virulence factor involved in the intestinal and hepatic phases of listeriosis. Begley, M. Contribution of three bile-associated loci, bsh, pva, and btlB, to gastrointestinal persistence and bile tolerance of Listeria monocytogenes.
Dowd, G. Investigation of the mechanisms by which Listeria monocytogenes grows in porcine gallbladder bile. Toledo-Arana, A. The Listeria transcriptional landscape from saprophytism to virulence. Mraheil, M. The intracellular sRNA transcriptome of Listeria monocytogenes during growth in macrophages.
Nucleic Acids Res. Listeria monocytogenes is a Gram-positive bacterium responsible for severe infections in human and a large variety of animal species. It is a facultative intracellular pathogen which invades macrophages and most tissue cells of infected hosts where it can proliferate.
The molecular basis of this intracellular parasitism has been to a large extent elucidated. Notably, immunization with LS compared to S-immunization, resulted in an additional 2-log increase in the reduction of bacterial burdens in the spleen and liver and complete elimination of bacterial colonization of the brain following challenge with LS Recently, a study from Europe on epidemic L.
Through specific genetic and genome-wide analyses, prior studies demonstrated that L. Since the characterization of these outbreak strains remains poorly studied, we investigated the pathogenicity and immune response to representative clinical isolates LS and LS compared to the commonly used L. We show that in vitro growth in broth culture for all of the outbreak strains and S is similar Fig.
Additional in vitro infection experiments indicated that the outbreak-associated strains have an enhanced ability to invade human cells and spread intracellularly Fig. Furthermore, the increase in invasion efficiencies of LS and LS were not attributed to an increase in flagellar motility compared to S Supplementary Fig. S2 However, at this time, we cannot rule out the possibility that differential expression of previously identified L. Despite the increase in invasion, the intracellular replication rate of the outbreak strains was similar to that of S Fig.
To understand the virulence differences between the outbreak-associated isolates and S, we conducted in vivo infection experiments in mice.
Infection of mice intravenously or orogastrically with LS or LS resulted in higher bacterial colonization in all mouse organs examined compared to infection with S Fig. These results suggest that the increased invasion and cell-to-cell spread capability of LS and LS Fig. Most notable was the level of colonization of the brain following the natural oral infection route Fig. These data suggest that the outbreak-associated strains are more efficient in mechanisms mediating crossing of the blood-brain barrier to infect the brain e.
Alternatively, an increase in the ability to survive and replicate within the infected host may lead to an overall increase in bacterial numbers that facilitates increased colonization of the brain in the absence of any specific enhanced mechanism of traversing the blood-brain barrier.
Nonetheless, the increased bacterial burden observed in all organs examined independent of the infection route Fig. While the specific gene determinants that mediate the increase in virulence of LS and LS compared to S are currently unknown, our respective sequence and hemolytic activity analyses of the principal virulence factors PrfA and LLO indicated no differences in protein sequence of PrfA Supplementary Fig.
Our studies do not preclude that expression differences or mutations in other identified or previously unknown virulence determinants play a role in the increased survival, invasion or cell-to-cell spread of the outbreak-associated strains.
Because of our determination that outbreak strain LS is genetically tractable Fig. Unfortunately, the complete genome sequences are not available for the L. However, comparative analyses between the genome sequences of L. LS and LS Although it is tempting to speculate that such genetic regions could play important roles in the pathogenesis of the outbreak strains, thorough experiments are needed to fully understand the basis of the increased virulence of the L.
This hypothesis may also be supported by the cross-strain protection studies Fig. These data indicated that in our mouse model of infection, pre-existing immunity to LS provides significant or equivalent reduction in bacterial burdens in organs following challenge with a lethal dose of S or LS Fig.
This result is consistent with data in Fig. In contrast, pre-existing immunity to S did not provide equivalent reduction in bacterial burdens following challenge with LS as observed following challenge with S Fig.
Most striking was the colonization of the brain in LSchallenged animals, where pre-existing immunity to S provided no measureable reduction in bacterial burden following LS challenge.
Collectively, these data Figs. If extrapolated to infections in humans, our results suggest that increased virulence in conjunction with a potential lack of protective immunity in the event of prior exposure to L. To our knowledge, this is the first report to characterize the pathogenesis and immune response of L. Furthermore, our data suggests that with respect to studies using L.
However, our studies highlight that widely used L. Further studies into the pathogenesis of the genetically tractable LS clinical isolate strain may allow a better understanding of the pathogenic mechanisms of L. All bacterial strains used in this study are listed in Supplementary Tables S1 and S2 in the Supplementary Information.
To generate an isogenic hly deletion mutant of L. Bone marrow-derived macrophages BMM were cultured as previously described On day 3, the culture medium was replaced with fresh BMM medium. On day 7, media was removed from the cells and BMM were harvested.
The indicated L. Twenty-four hours later, plaques were imaged and the relative plaque diameters were measured. To analyze the flagellar motility of L. For animal infections with L. Each group included 4 mice and experiments were repeated twice.
Mice were monitored twice daily for signs of disease and moribund animals were euthanized on day 3 post-infection. Surviving mice were monitored twice daily for an additional seven days for signs of disease and moribund animals were euthanized. All animal care and experiments were conducted in compliance with the Association for Assessment and Accreditation of Laboratory Animal Care regulations. All experimental protocols were approved by the Harvard Medical School Institutional Animal Care and Use Committee and were in compliance with all federal, state and local laws.
Mice were monitored daily for signs of disease after immunization. Mice were monitored twice daily for signs of disease. Briefly, two-fold serial dilutions of culture supernatants were made in PBS pH 5.
The assay was repeated 5 times with duplicates. Statistical analysis for in vivo virulence studies was performed using the Mann-Whitney U-test.
Radoshevich, L. Listeria monocytogenes : towards a complete picture of its physiology and pathogenesis. Vazquez-Boland, J. Listeria pathogenesis and molecular virulence determinants. Thigpen, M. Bacterial meningitis in the United States, — Listeria placental infection. The global burden of listeriosis: a systematic review and meta-analysis. Lancet Infect. Cartwright, E. Listeriosis outbreaks and associated food vehicles, United States, — Google Scholar.
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