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Clinical Microbiology Reviews Mar 2023Listeria monocytogenes is a Gram-positive facultative intracellular pathogen that can cause severe invasive infections upon ingestion with contaminated food. Clinically,... (Review)
Review
Listeria monocytogenes is a Gram-positive facultative intracellular pathogen that can cause severe invasive infections upon ingestion with contaminated food. Clinically, listerial disease, or listeriosis, most often presents as bacteremia, meningitis or meningoencephalitis, and pregnancy-associated infections manifesting as miscarriage or neonatal sepsis. Invasive listeriosis is life-threatening and a main cause of foodborne illness leading to hospital admissions in Western countries. Sources of contamination can be identified through international surveillance systems for foodborne bacteria and strains' genetic data sharing. Large-scale whole genome studies have increased our knowledge on the diversity and evolution of L. monocytogenes, while recent pathophysiological investigations have improved our mechanistic understanding of listeriosis. In this article, we present an overview of human listeriosis with particular focus on relevant features of the causative bacterium, epidemiology, risk groups, pathogenesis, clinical manifestations, and treatment and prevention.
Topics: Pregnancy; Female; Infant, Newborn; Humans; Listeriosis; Listeria monocytogenes; Risk Factors; Bacteremia; Food Microbiology
PubMed: 36475874
DOI: 10.1128/cmr.00060-19 -
Virulence Dec 2020Listeriosis is a rare and severe foodborne infection caused by . It manifests as septicemia, neurolisteriosis, and maternal-fetal infection. In pregnancy, it may cause... (Review)
Review
Listeriosis is a rare and severe foodborne infection caused by . It manifests as septicemia, neurolisteriosis, and maternal-fetal infection. In pregnancy, it may cause maternal fever, premature delivery, fetal loss, neonatal systemic and central nervous system infections. Maternal listeriosis is mostly reported during the 2nd and 3rd trimester of pregnancy, as sporadic cases or in the context of outbreaks. Strains belonging to clonal complexes 1, 4 and 6, referred to as hypervirulent, are the most associated to maternal-neonatal infections. Here we review the clinical, pathophysiological, and microbiological features of maternal-neonatal listeriosis.
Topics: Animals; Female; Humans; Infant, Newborn; Infant, Newborn, Diseases; Infectious Disease Transmission, Vertical; Listeria monocytogenes; Listeriosis; Mice; Placenta; Pregnancy; Pregnancy Complications, Infectious; Risk Factors
PubMed: 32363991
DOI: 10.1080/21505594.2020.1759287 -
Cellular Microbiology Apr 2020Listeria monocytogenes causes listeriosis, a systemic infection which manifests as bacteremia, often complicated by meningoencephalitis in immunocompromised individuals... (Review)
Review
Listeria monocytogenes causes listeriosis, a systemic infection which manifests as bacteremia, often complicated by meningoencephalitis in immunocompromised individuals and the elderly, and fetal-placental infection in pregnant women. It has emerged over the past decades as a major foodborne pathogen, responsible for numerous outbreaks in Western countries, and more recently in Africa. L. monocytogenes' pathogenic properties have been studied in detail, thanks to concomitant advances in biological sciences, in particular molecular biology, cell biology and immunology. L. monocytogenes has also been instrumental to basic advances in life sciences. L. monocytogenes therefore stands both a tool to understand biology and a model in infection biology. This review briefly summarises the clinical and some of the pathophysiological features of listeriosis. In the context of this special issue, it highlights some of the major discoveries made by Pascale Cossart in the fields of molecular and cellular microbiology since the mid-eighties regarding the identification and characterisation of multiple bacterial and host factors critical to L. monocytogenes pathogenicity. It also briefly summarises some of the key findings from our laboratory on this topic over the past years.
Topics: Animals; Food Microbiology; Host-Pathogen Interactions; Humans; Listeria monocytogenes; Listeriosis; Mice; Sepsis
PubMed: 32185900
DOI: 10.1111/cmi.13186 -
Trends in Microbiology Sep 2021Listeria monocytogenes is a foodborne pathogen responsible for listeriosis, an infection that can manifest in humans as bacteremia, meningoencephalitis in... (Review)
Review
Listeria monocytogenes is a foodborne pathogen responsible for listeriosis, an infection that can manifest in humans as bacteremia, meningoencephalitis in immunocompromised patients and the elderly, and fetal-placental infection in pregnant women. Reference strains from this facultative intracellular bacterium have been instrumental in the investigation of basic mechanisms in microbiology, immunology, and cell biology. The integration of bacterial population genomics with environmental, epidemiological, and clinical data allowed the uncovering of new factors involved in the virulence of L. monocytogenes and its adaptation to different environments. This review illustrates how these investigations have led to a better understanding of the bacterium's virulence and the driving forces that shaped it.
Topics: Adaptation, Physiological; Animals; Biodiversity; Humans; Listeria monocytogenes; Listeriosis; Virulence
PubMed: 33583696
DOI: 10.1016/j.tim.2021.01.008 -
Molecular Cell Feb 2022Citrulline can be converted into argininosuccinate by argininosuccinate synthetase (ASS1) in the urea cycle and the citrulline-nitric oxide cycle. However, the...
Citrulline can be converted into argininosuccinate by argininosuccinate synthetase (ASS1) in the urea cycle and the citrulline-nitric oxide cycle. However, the regulation and biological function of citrulline metabolism remain obscure in the immune system. Unexpectedly, we found that macrophage citrulline declines rapidly after interferon gamma (IFN-γ) and/or lipopolysaccharide (LPS) stimulation, which is required for efficient proinflammatory signaling activation. Mechanistically, IFN-γ and/or LPS stimulation promotes signal transducers and activators of transcription 1 (STAT1)-mediated ASS1 transcription and Janus kinase2 (JAK2)-mediated phosphorylation of ASS1 at tyrosine 87, thereby leading to citrulline depletion. Reciprocally, increased citrulline directly binds to JAK2 and inhibits JAK2-STAT1 signaling. Blockage of ASS1-mediated citrulline depletion suppresses the host defense against bacterial infection in vivo. We therefore define a central role for ASS1 in controlling inflammatory macrophage activation and antibacterial defense through depletion of cellular citrulline and, further, identify citrulline as an innate immune-signaling metabolite that engages a metabolic checkpoint for proinflammatory responses.
Topics: Animals; Argininosuccinate Synthase; Citrulline; Disease Models, Animal; HEK293 Cells; Humans; Immunity, Innate; Inflammation; Inflammation Mediators; Janus Kinase 2; Listeria monocytogenes; Listeriosis; Macrophage Activation; Macrophages; Mice; Mice, Inbred C57BL; Mice, Knockout; Phosphorylation; RAW 264.7 Cells; STAT1 Transcription Factor; Signal Transduction
PubMed: 35016033
DOI: 10.1016/j.molcel.2021.12.006 -
Science (New York, N.Y.) Jan 2021Infection triggers expansion and effector differentiation of T cells specific for microbial antigens in association with metabolic reprograming. We found that the...
Infection triggers expansion and effector differentiation of T cells specific for microbial antigens in association with metabolic reprograming. We found that the glycolytic enzyme lactate dehydrogenase A (LDHA) is induced in CD8 T effector cells through phosphoinositide 3-kinase (PI3K) signaling. In turn, ablation of LDHA inhibits PI3K-dependent phosphorylation of Akt and its transcription factor target Foxo1, causing defective antimicrobial immunity. LDHA deficiency cripples cellular redox control and diminishes adenosine triphosphate (ATP) production in effector T cells, resulting in attenuated PI3K signaling. Thus, nutrient metabolism and growth factor signaling are highly integrated processes, with glycolytic ATP serving as a rheostat to gauge PI3K-Akt-Foxo1 signaling in the control of T cell immunity. Such a bioenergetic mechanism for the regulation of signaling may explain the Warburg effect.
Topics: Animals; CD8-Positive T-Lymphocytes; Forkhead Box Protein O1; Glycolysis; Humans; Lactate Dehydrogenase 5; Listeria monocytogenes; Listeriosis; Mice; Mice, Mutant Strains; Phosphatidylinositol 3-Kinase; Phosphorylation; Proto-Oncogene Proteins c-akt; Signal Transduction; Warburg Effect, Oncologic
PubMed: 33479154
DOI: 10.1126/science.abb2683 -
Microbiology Spectrum Jul 2019Bacterial metabolism represents the biochemical space that bacteria can manipulate to produce energy, reducing equivalents and building blocks for replication.... (Review)
Review
Bacterial metabolism represents the biochemical space that bacteria can manipulate to produce energy, reducing equivalents and building blocks for replication. Gram-positive pathogens, such as , show remarkable flexibility, which allows for exploitation of diverse biological niches from the soil to the intracytosolic space. Although the human host represents a potentially rich source for nutrient acquisition, competition for nutrients with the host and hostile host defenses can constrain bacterial metabolism by various mechanisms, including nutrient sequestration. Here, we review metabolism in the model Gram-positive bacterium, , and highlight pathways that enable the replication, survival, and virulence of this bacterial pathogen.
Topics: Animals; Bacterial Proteins; Gene Expression Regulation, Bacterial; Humans; Listeria monocytogenes; Listeriosis; Virulence
PubMed: 31418407
DOI: 10.1128/microbiolspec.GPP3-0066-2019 -
Science (New York, N.Y.) Feb 2022Group 3 innate lymphoid cells (ILC3s) are innate immune effectors that contribute to host defense. Whether ILC3 functions are stably modified after pathogen encounter is...
Group 3 innate lymphoid cells (ILC3s) are innate immune effectors that contribute to host defense. Whether ILC3 functions are stably modified after pathogen encounter is unknown. Here, we assess the impact of a time-restricted enterobacterial challenge to long-term ILC3 activation in mice. We found that intestinal ILC3s persist for months in an activated state after exposure to . Upon rechallenge, these "trained" ILC3s proliferate, display enhanced interleukin-22 (IL-22) responses, and have a superior capacity to control infection compared with naïve ILC3s. Metabolic changes occur in -exposed ILC3s, but only trained ILC3s have an enhanced proliferative capacity that contributes to increased IL-22 production. Accordingly, a limited encounter with a pathogen can promote durable phenotypic and functional changes in intestinal ILC3s that contribute to long-term mucosal defense.
Topics: Adaptive Immunity; Animals; Cell Proliferation; Citrobacter rodentium; Enterobacteriaceae Infections; Female; Immunity, Innate; Immunity, Mucosal; Immunologic Memory; Interleukins; Intestinal Mucosa; Intestines; Listeria monocytogenes; Listeriosis; Lymphocyte Activation; Lymphocytes; Male; Metabolic Networks and Pathways; Mice; Mice, Inbred C57BL; Oxygen Consumption; RNA-Seq; Reinfection; Interleukin-22
PubMed: 35201883
DOI: 10.1126/science.aaz8777 -
Nature Communications Oct 2022Listeria monocytogenes is a foodborne intracellular bacterial pathogen leading to human listeriosis. Despite a high mortality rate and increasing antibiotic resistance...
Listeria monocytogenes is a foodborne intracellular bacterial pathogen leading to human listeriosis. Despite a high mortality rate and increasing antibiotic resistance no clinically approved vaccine against Listeria is available. Attenuated Listeria strains offer protection and are tested as antitumor vaccine vectors, but would benefit from a better knowledge on immunodominant vector antigens. To identify novel antigens, we screen for Listeria peptides presented on the surface of infected human cell lines by mass spectrometry-based immunopeptidomics. In between more than 15,000 human self-peptides, we detect 68 Listeria immunopeptides from 42 different bacterial proteins, including several known antigens. Peptides presented on different cell lines are often derived from the same bacterial surface proteins, classifying these antigens as potential vaccine candidates. Encoding these highly presented antigens in lipid nanoparticle mRNA vaccine formulations results in specific CD8 T-cell responses and induces protection in vaccination challenge experiments in mice. Our results can serve as a starting point for the development of a clinical mRNA vaccine against Listeria and aid to improve attenuated Listeria vaccines and vectors, demonstrating the power of immunopeptidomics for next-generation bacterial vaccine development.
Topics: Animals; Bacterial Proteins; Bacterial Vaccines; CD8-Positive T-Lymphocytes; Humans; Immunodominant Epitopes; Liposomes; Listeria; Listeria monocytogenes; Listeriosis; Membrane Proteins; Mice; Nanoparticles; Vaccines, Attenuated; Vaccines, Synthetic; mRNA Vaccines
PubMed: 36241641
DOI: 10.1038/s41467-022-33721-y -
Nature Feb 2021In contrast to nearly all other tissues, the anatomy of cell differentiation in the bone marrow remains unknown. This is owing to a lack of strategies for examining...
In contrast to nearly all other tissues, the anatomy of cell differentiation in the bone marrow remains unknown. This is owing to a lack of strategies for examining myelopoiesis-the differentiation of myeloid progenitors into a large variety of innate immune cells-in situ in the bone marrow. Such strategies are required to understand differentiation and lineage-commitment decisions, and to define how spatial organizing cues inform tissue function. Here we develop approaches for imaging myelopoiesis in mice, and generate atlases showing the differentiation of granulocytes, monocytes and dendritic cells. The generation of granulocytes and dendritic cells-monocytes localizes to different blood-vessel structures known as sinusoids, and displays lineage-specific spatial and clonal architectures. Acute systemic infection with Listeria monocytogenes induces lineage-specific progenitor clusters to undergo increased self-renewal of progenitors, but the different lineages remain spatially separated. Monocyte-dendritic cell progenitors (MDPs) map with nonclassical monocytes and conventional dendritic cells; these localize to a subset of blood vessels expressing a major regulator of myelopoiesis, colony-stimulating factor 1 (CSF1, also known as M-CSF). Specific deletion of Csf1 in endothelium disrupts the architecture around MDPs and their localization to sinusoids. Subsequently, there are fewer MDPs and their ability to differentiate is reduced, leading to a loss of nonclassical monocytes and dendritic cells during both homeostasis and infection. These data indicate that local cues produced by distinct blood vessels are responsible for the spatial organization of definitive blood cell differentiation.
Topics: Animals; Atlases as Topic; Blood Vessels; Cell Lineage; Cell Self Renewal; Cell Tracking; Dendritic Cells; Endothelium, Vascular; Female; Granulocytes; Listeria monocytogenes; Listeriosis; Macrophage Colony-Stimulating Factor; Male; Mice; Monocytes; Myeloid Cells; Myelopoiesis; Staining and Labeling
PubMed: 33568812
DOI: 10.1038/s41586-021-03201-2