ArticleInfection and immunity2008
Listeria monocytogenes desensitizes immune cells to subsequent Ca2+ signaling via listeriolysin O-induced depletion of intracellular Ca2+ stores.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- The Multifaceted Role of Calcium Signaling in Regulated Necrosis.Biomolecules · 2025Review
- Pathogenesis of Multiple Organ Failure: The Impact of Systemic Damage to Plasma Membranes.Frontiers in medicine · 2022Review
- Beyond pore formation: reorganization of the plasma membrane induced by pore-forming proteins.Cellular and molecular life sciences : CMLS · 2021Review
- Bacterial Toxins Are a Never-Ending Source of Surprises: From Natural Born Killers to Negotiators.Toxins · 2021Review
- Tauroursodeoxycholic acid prevents Burkholderia pseudomallei-induced endoplasmic reticulum stress and is protective during melioidosis in mice.BMC microbiology · 2021Article
- Hiding in Plain Sight: Formation and Function of Stress Granules During Microbial Infection of Mammalian Cells.Frontiers in molecular biosciences · 2021Review
- Impact of Bacterial Toxins in the Lungs.Toxins · 2020Review
- Stress Response ofFrontiers in microbiology · 2020Article
- Mechanisms protecting host cells against bacterial pore-forming toxins.Cellular and molecular life sciences : CMLS · 2019Review
- Review
- Cellular Stress Responses and Gut Microbiota in Inflammatory Bowel Disease.Gastroenterology research and practice · 2018Review
- Regulation of Cytokine Production by the Unfolded Protein Response; Implications for Infection and Autoimmunity.Frontiers in immunology · 2018Review
- Pseudomonas aeruginosa ExlA and Serratia marcescens ShlA trigger cadherin cleavage by promoting calcium influx and ADAM10 activation.PLoS pathogens · 2017Article
- Plasticity of listeriolysin O pores and its regulation by pH and unique histidine [corrected].Scientific reports · 2015Article
- Bacteria, the endoplasmic reticulum and the unfolded protein response: friends or foes?Nature reviews. Microbiology · 2015Review
- Listeriolysin O Affects the Permeability of Caco-2 Monolayer in a Pore-Dependent and Ca2+-Independent Manner.PloS one · 2015Article
- Fluxes of Ca2+ and K+ are required for the listeriolysin O-dependent internalization pathway of Listeria monocytogenes.Infection and immunity · 2014Article
- Multifaceted activity of listeriolysin O, the cholesterol-dependent cytolysin of Listeria monocytogenes.Sub-cellular biochemistry · 2014Review
- Metabolic host responses to infection by intracellular bacterial pathogens.Frontiers in cellular and infection microbiology · 2013Review
- IL-1 receptor regulates S100A8/A9-dependent keratinocyte resistance to bacterial invasion.Mucosal immunology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Listeriolysin O (LLO), the pore-forming toxin of Listeria monocytogenes, is a prototype of the cholesterol-dependent cytolysins (CDCs) secreted by several pathogenic and nonpathogenic gram-positive bacteria. In addition to mediating the escape of the bacterium into the cytosol, this toxin is generally believed to be a central player in host-pathogen interactions during L. monocytogenes infection. LLO triggers the influx of Ca(2+) into host cells as well as the release of Ca(2+) from intracellular stores. Thus, many of the cellular responses induced by LLO are related to calcium signaling. Interestingly, in this study, we report that prolonged exposure to LLO desensitizes cells to Ca(2+) mobilization upon subsequent stimulations with LLO. Cells preexposed to LLO-positive L. monocytogenes but not to the LLO-deficient Deltahly mutant were found to be highly refractory to Ca(2+) induction in response to receptor-mediated stimulation. Such cells also exhibited diminished Ca(2+) signals in response to stimulation with LLO and thapsigargin. The presented results suggest that this phenomenon is due to the depletion of intracellular Ca(2+) stores. The ability of LLO to desensitize immune cells provides a significant hint about the possible role played by CDCs in the evasion of the immune system by bacterial pathogens.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.