Caspase-7 activation by the Nlrc4/Ipaf inflammasome restricts Legionella pneumophila infection, PLoS Pathog, vol.5, p.1000361, 2009. ,
Staphylococcus aureus-induced G2/M phase transition delay in host epithelial cells increases bacterial infective efficiency, PLoS One, vol.8, 2013. ,
URL : https://hal.archives-ouvertes.fr/hal-00873672
, , 2018.
A link between osteomyelitis and IL1RN and IL1B polymorphisms-a study in patients from Northeast Brazil, Acta Orthop, vol.88, pp.556-561, 2017. ,
Regulation of Legionella phagosome maturation and infection through flagellin and host Ipaf, J Biol Chem, vol.281, pp.35217-35223, 2006. ,
URL : https://hal.archives-ouvertes.fr/hal-01936389
Aspergillus fumigatus conidia inhibit tumour necrosis factor-or staurosporine-induced apoptosis in epithelial cells, Int Immunol, vol.18, pp.139-150, 2006. ,
Inhibition of Staphylococcus aureus invasion into bovine mammary epithelial cells by contact with live Lactobacillus casei, Appl Environ Microbiol, vol.79, pp.877-885, 2013. ,
URL : https://hal.archives-ouvertes.fr/hal-01454235
Inflammasomes: intracellular detection of extracellular bacteria, Cell Res, vol.26, pp.859-860, 2016. ,
Inflammasomes: mechanism of assembly, regulation and signalling, Nat Rev Immunol, vol.16, pp.407-420, 2016. ,
Dectin-2 is a primary receptor for NLRP3 inflammasome activation in dendritic cell response to Histoplasma capsulatum, PLoS Pathog, vol.13, p.1006485, 2017. ,
SERPINB1-mediated checkpoint of inflammatory caspase activation, Nat Immunol, vol.20, pp.276-287, 2019. ,
, , 2018.
, S. aureus evades macrophage killing through NLRP3-dependent effects on mitochondrial trafficking, Cell Rep, vol.22, pp.2431-2441
Infection associated with prosthetic Joints, N Engl J Med, vol.361, pp.787-794, 2009. ,
Staphylococcus aureus Phenol-Soluble Modulins Impair Interleukin Expression in Bovine Mammary Epithelial Cells, Infect Immun, vol.84, pp.1682-1692, 2016. ,
URL : https://hal.archives-ouvertes.fr/hal-01352689
Phenolsoluble modulin ? induces G2/M phase transition delay in eukaryotic HeLa cells, FASEB J, vol.29, pp.1950-1959, 2015. ,
Staphylococcus aureus induces DNA damage in host cell, Sci Rep, vol.9, p.7694, 2019. ,
URL : https://hal.archives-ouvertes.fr/hal-02153435
Treating inflammation by blocking interleukin-1 in a broad spectrum of diseases, Nat Rev Drug Discov, vol.11, pp.633-652, 2012. ,
Caspase-1zeta, a new splice variant of the caspase-1 gene, Genomics, vol.84, pp.587-591, 2004. ,
The pyroptosome: a supramolecular assembly of ASC dimers mediating inflammatory cell death via caspase-1 activation, Cell Death Differ, vol.14, pp.1590-1604, 2007. ,
Intracellular replication of Staphylococcus aureus in mature phagolysosomes in macrophages precedes host cell death, and bacterial escape and dissemination, Cell Microbiol, vol.18, pp.514-535, 2016. ,
NLRC4-driven production of IL-1? discriminates between pathogenic and commensal bacteria and promotes host intestinal defense, Nat Immunol, vol.13, pp.449-456, 2012. ,
Expression of ?-toxin by Staphylococcus aureus mediates escape from phago-endosomes of human epithelial and endothelial cells in the presence of ?-toxin, Cellular Microbiology, vol.13, pp.316-329, 2011. ,
A noncoding function of TYRP1 mRNA promotes melanoma growth, Nat Cell Biol, vol.19, pp.1348-1357, 2017. ,
URL : https://hal.archives-ouvertes.fr/hal-01647130
Pharmacological characterization of ATP-and LPS-induced IL-1beta release in human monocytes, Br J Pharmacol, vol.127, pp.1915-1921, 1999. ,
Caspase-1 activation of lipid metabolic pathways in response to bacterial pore-forming toxins promotes cell survival, Cell, vol.126, pp.1135-1145, 2006. ,
Repair of global regulators in Staphylococcus aureus 8325 and comparative analysis with other clinical isolates, Infect Immun, vol.78, pp.2877-2889, 2010. ,
Lose the battle to win the war: bacterial strategies for evading host inflammasome activation, Trends Microbiol, vol.21, pp.342-349, 2013. ,
Two restriction and modification systems in Staphylococcus aureus NCTC8325, J Gen Microbiol, vol.96, pp.277-281, 1976. ,
Phagocytosis and phagosome acidification are required for pathogen processing and MyD88-dependent responses to Staphylococcus aureus, J Immunol, vol.184, pp.7071-7081, 2010. ,
The isolation and analysis of phenol-soluble modulins of Staphylococcus epidermidis, Methods Mol Biol, vol.1106, pp.93-100, 2014. ,
Staphylococcus aureus vs. Osteoblast: Relationship and Consequences in Osteomyelitis, Front Cell Infect Microbiol, vol.5, 2015. ,
URL : https://hal.archives-ouvertes.fr/hal-02163998
Clinical Significance and Pathogenesis of Staphylococcal Small Colony Variants in Persistent Infections, Clin Microbiol Rev, vol.29, pp.401-427, 2016. ,
Drug release and bone growth studies of antimicrobial peptide-loaded calcium phosphate coating on titanium, J Biomed Mater Res Part B Appl Biomater, vol.100, pp.1344-1352, 2012. ,
Evidence for interleukin-1 beta production by cultured normal human osteoblast-like cells, J Bone Miner Res, vol.6, pp.827-833, 1991. ,
Active caspase-1 is a regulator of unconventional protein secretion, Cell, vol.132, pp.818-831, 2008. ,
Mineral trioxide aggregate stimulates a biological response in human osteoblasts, J Biomed Mater Res, vol.37, pp.432-439, 1997. ,
Frontline Science: Staphylococcus aureus promotes receptor-interacting protein kinase 3-and protease-dependent production of IL-1? in human neutrophils, J Leukoc Biol, vol.105, pp.437-447, 2019. ,
, The Inflammasomes. PLOS Pathogens, vol.5, p.1000510, 2009.
Mechanisms and functions of inflammasomes, Cell, vol.157, pp.1013-1022, 2014. ,
IL-1 plays an important role in the bone metabolism under physiological conditions, Int Immunol, vol.22, pp.805-816, 2010. ,
Inflammasome-derived IL-1? production induces nitric oxide-mediated resistance to Leishmania, Nat Med, vol.19, pp.909-915, 2013. ,
Molecular pathogenesis of Staphylococcus aureus infection, Pediatr Res, vol.65, pp.71-77, 2009. ,
Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method, Methods, vol.25, pp.402-408, 2001. ,
Understanding the mechanism of IL-1? secretion, Cytokine Growth Factor Rev, vol.22, pp.189-195, 2011. ,
LncRNA XIST mediates bovine mammary epithelial cell inflammatory response via NF-?B/NLRP3 inflammasome pathway, Cell Prolif, vol.52, p.12525, 2019. ,
RNA-guided human genome engineering via Cas9, Science, vol.339, pp.823-826, 2013. ,
Inflammasomes coordinate pyroptosis and natural killer cell cytotoxicity to clear infection by a ubiquitous environmental bacterium, Immunity, vol.43, pp.987-997, 2015. ,
Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf, Nature, vol.430, pp.213-218, 2004. ,
Bacterial infection of osteoblasts induces interleukin-1beta and interleukin-18 transcription but not protein synthesis, J Interferon Cytokine Res, vol.22, pp.1049-1055, 2002. ,
Mycobacterium tuberculosis prevents inflammasome activation, Cell Host Microbe, vol.3, pp.224-232, 2008. ,
Pyrin N-terminal homology domain-and caspase recruitment domain-dependent oligomerization of ASC, Biochem Biophys Res Commun, vol.280, pp.652-655, 2001. ,
WIPI-1 positive autophagosome-like vesicles entrap athogenic Staphylococcus aureus for lysosomal degradation, Int J Cell Biol, p.179207, 2012. ,
Staphylococcus aureus activates the NLRP3 inflammasome in human and rat conjunctival goblet cells, PLoS ONE, vol.8, p.74010, 2013. ,
Synovial fluid concentrations and relative potency of interleukin-1 alpha and beta in cartilage and meniscus degradation, J Orthop Res, vol.31, pp.1039-1045, 2013. ,
Inflammasomemediated production of IL-1beta is required for neutrophil recruitment against Staphylococcus aureus in vivo, J Immunol, vol.179, pp.6933-6942, 2007. ,
Intracellular proliferation of S. aureus in osteoblasts and effects of rifampicin and gentamicin on S. aureus intracellular proliferation and survival, Eur Cell Mater, vol.28, pp.258-268, 2014. ,
A type I IFN-dependent DNA damage response regulates the genetic program and inflammasome activation in macrophages, 2017. ,
Staphylococcus aureus Lpl lipoproteins delay G2/M phase transition in HeLa cells, Front Cell Infect Microbiol, vol.6, 2016. ,
URL : https://hal.archives-ouvertes.fr/hal-01423207
Basis of virulence in community-associated methicillin-resistant Staphylococcus aureus, Annu Rev Microbiol, vol.64, pp.143-162, 2010. ,
How Staphylococcus aureus biofilms develop their characteristic structure, Proc Natl Acad Sci, vol.109, pp.1281-1286, 2012. ,
Systems-level interference strategies to decipher host factors involved in bacterial pathogen interaction: from RNAi to CRISPRi, Curr Opin Microbiol, vol.39, pp.34-41, 2017. ,
RNAIII-independent target gene control by the agr quorum-sensing system: insight into the evolution of virulence regulation in Staphylococcus aureus, Mol Cell, vol.32, pp.150-158, 2008. ,
Caspase-1-mediated activation of interleukin-1beta (IL-1beta) and IL-18 contributes to innate immune defenses against >Salmonella enterica</i> serovar Typhimurium infection, Infect Immun, vol.74, pp.4922-4926, 2006. ,
Induction of macrophage function in human THP-1 cells Is associated with rewiring of MAPK signaling and activation of MAP3K7 (TAK1) protein kinase, Front Cell Dev Biol, vol.4, p.21, 2016. ,
Innate cell communication kick-starts pathogen-specific immunity, Nat Immunol, vol.17, pp.356-363, 2016. ,
The role of IL-1? in the bone loss during rheumatic diseases, Mediators Inflamm, p.782382, 2015. ,
Improved vectors and genome-wide libraries for CRISPR screening, Nat Methods, vol.11, pp.783-784, 2014. ,
Caspase-4 mediates non-canonical activation of the NLRP3 inflammasome in human myeloid cells, Eur J Immunol, vol.45, pp.2911-2917, 2015. ,
The inflammasomes, Cell, vol.140, pp.821-832, 2010. ,
Serratiopeptidase reduces the invasion of osteoblasts by Staphylococcus aureus, Int J Immunopathol Pharmacol, vol.30, pp.423-428, 2017. ,
Staphylococcus aureus evades lysozyme-based peptidoglycan digestion that links phagocytosis, inflammasome activation, and IL-1beta secretion, Cell Host Microbe, vol.7, pp.38-49, 2010. ,
The Inflammasome and the Epidermal Growth Factor Receptor (EGFR) Are Involved in the Staphylococcus aureus-Mediated Induction of IL-1alpha and IL-1beta in Human Keratinocytes, PLoS ONE, vol.11, 2016. ,
Activation of caspase-1 by the NLRP3 inflammasome regulates the NADPH oxidase NOX2 to control phagosome function, Nat Immunol, vol.14, pp.543-553, 2013. ,
Caspase-1: the inflammasome and beyond, Innate Immun, vol.20, pp.115-125, 2014. ,
PMA withdrawal in PMA-treated monocytic THP-1 cells and subsequent retinoic acid stimulation, modulate induction of apoptosis and appearance of dendritic cells, Cell Prolif, vol.46, pp.328-347, 2013. ,
Inflammasomes in health and disease, Nature, vol.481, pp.278-286, 2012. ,
Staphlyococcus aureus phenol-soluble modulins stimulate the release of proinflammatory cytokines from keratinocytes and are required for induction of skin inflammation, Infect Immun, vol.83, pp.3428-3437, 2015. ,
Staphylococcus aureus Infections: epidemiology, pathophysiology, clinical manifestations, and management, Clin Microbiol Rev, vol.28, pp.603-661, 2015. ,
Adaptive processes of Staphylococcus aureus isolates during the progression from acute to chronic bone and joint infections in patients, Cell Microbiol, vol.18, pp.1405-1414, 2016. ,
URL : https://hal.archives-ouvertes.fr/hal-01377319
Staphylococcus aureus phenotype switching: an effective bacterial strategy to escape host immune response and establish a chronic infection, EMBO Mol Med, vol.3, pp.129-141, 2011. ,
, , 2015.
, Antimicrobial Activity against Intraosteoblastic Staphylococcus aureus. Antimicrob Agents Chemother, vol.59, pp.2029-2036
Human caspase-4 and caspase-5 regulate the one-step non-canonical inflammasome activation in monocytes, Nat Commun, vol.6, 2015. ,
Inflammasomes and host defenses against bacterial infections, Curr Opin Microbiol, vol.16, pp.23-31, 2013. ,
Investigational drugs to treat methicillinresistant Staphylococcus aureus, Expert Opin Investig Drugs, vol.25, pp.73-93, 2016. ,
Identification of novel cytolytic peptides as key virulence determinants for community-associated MRSA, Nature Medicine, vol.13, pp.1510-1514, 2007. ,
Regulation of chemokine gene expression and secretion in Staphylococcus aureus-infected osteoblasts, Microbes Infect, vol.6, pp.844-852, 2004. ,
PKR induces the expression of NLRP3 by regulating the NF-?B pathway in Porphyromonas gingivalisinfected osteoblasts, Exp Cell Res, vol.354, pp.57-64, 2017. ,
Salmonella exploits NLRP12-dependent innate immune signaling to suppress host defenses during infection, Proc Natl Acad Sci, vol.111, pp.385-390, 2014. ,
Transmission electron micrographs of MG-63 cells infected with MW2 strain at MOI 50:1 for indicated time points. MG-63 cells were fixed as described in Experimental procedures. The pellets were mixed with 3% agar in sodium cacodylate, embedded in Epon-Araldite-DMP30 resin mixture and polymerized for 48 h. Sections were cut in Leica ultra microtome, Annals of Translational Medicine, vol.7, 2019. ,
, Images were digitally captured with GATAN Orius camera (Digital Micrograph Software). Magnification x12,000, scale bar: 1 µm
, speck-like aggregate formation and IL-1? secretion by WT MG-63 vs CASP1 -/-MG-63 cells exposed to S. aureus A. Analysis of mRNA levels of NLRP3 in WT MG-63
, MG-63 and CASP1 -/-MG-63 G2 cells were treated with 1 mg/mL ATP for 30 min
MG-63 or CASP1 -/-MG-63 G2 cells were exposed to S. aureus LAC (USA300) for 2 h. Following fixation and permeabilization of cells, NLRP3 expression at the protein level was determined by FACS using Rat Anti-Human NLRP3 ,
, Alexa Fluor® 488-conjugated Monoclonal Antibody or isotype control antibody (blue colour) per 10 6 cells. NLRP3 protein expression of untreated (red colour) or infected (black colour) cells were analyzed with an Accuri C6 flow cytometer. Data were collected from 20,000 cells, and analyzed with CFlow software
, The major density of events is captured by the gate. The events that represent debris, cell fragments and pyknotic cells are eliminated. Values shown on the right side of the graph refer to the respective mean fluorescence intensities (MFIs), Cells are analyzed using FSC-A x SSC-A plot, vol.50
63 or CASP1 -/-MG-63 cells were exposed to 1 ?g/mL LPS for 30 min and to 5 mM ATP for 15 min (LPS+ATP) (D) or to S, vol.50, p.1 ,
, Six hours post-infection cells were immunostained with rabbit anti PYCARD antibody (Coger France), followed by incubation with Alexa Fluor 488 labeled goat anti-rabbit antibody (Cell Signaling Ozyme) at a dilution of 1:20 for 2 h at room temperature (green staining, green arrows). Nuclear DNA was labeled with DAPI (blue staining). Samples were viewed with a Zeiss laser-scanning microscope equipped with a 63 × plan Apo-NA 1.4 immersion objective driven by Zen software, A. WT MG-63 or CASP1 -/-MG-63 cells were exposed to a fluorescent derivative of S. aureus SA113, which carries plasmid-encoded mCherry (red fluorescence, red arrows)
MG-63 or CASP1 -/-MG-63 G2 cells were exposed to S. aureus SA113 at MOI 50:1 for 6 h. To quantify the amount of ASC-speck forming cells the number of ASC speck out of 100 cells in the culture of WT MG-63 cells vs CASP1 -/-MG-63 G2 clone was enumerated. The results from three ,
MG-63 or CASP1 -/-MG-63 cells were exposed to S. aureus MW2 strain at MOI 50:1 for 2 h followed by antibiotic treatment as described. Six hours post-infection cells were lysed with 0.05% Triton X-100 in PBS, cell lysates were plated on BHI agar, and CFU were determined after overnight incubation ,
, After various times post-infection (6 h, 2 days, 5 days, 7, days and 11 days) cell supernatants were collected, centrifuged and the level of IL-1? was determined by a sandwich-ELISA (Thermofischer Life Technologies) as described in Experimental procedures. The values are presented as concentrations in pg/mL. Three independent assays were performed. The differences among the groups were assessed by the analysis of variance (ANOVA). P-values < 0.05 ( ? ) were considered to be significant. Tukey's Honestly Significant Difference test was applied for comparison of means between the groups, Figure 6. S. aureus strain-dependent release of IL-1? by infected MG-63 cells A
MG-63 cells were exposed to S. aureus strains LAC (USA300, p.2 ,
, After various times post-infection (6 h, 2 days, 5 days, 7, days and 11 days) cell supernatants were collected, centrifuged and the level of IL-1? was determined by a commercial sandwich-ELISA (Invitrogen, France) as described in Experimental procedures. The values are presented as concentrations in pg/mL. Three independent assays were performed. The differences among the groups were assessed by analysis of variance (ANOVA)
After various time post-infection (2 days and 5 days) cell supernatants were collected, centrifuged and the level of IL-1? was determined by a sandwich-ELISA (Thermofischer Life Technologies) as described in Experimental procedures. The IL-1? values are presented as concentrations in pg/mL ,
, Tukey's Honestly Significant Difference test was applied for comparison of means between the groups. The values are expressed as means ± standard deviation (±SD)
, ( ? ) were considered to be significant. Three independent assays were performed
MG-63 cells were exposed to USA300 LAC (pTX?16), which carries the control plasmid, the deletion mutant LAC?psm??hld (pTX?16) and the complemented strains expressing the four PSM? peptides (LAC?psm??hld-pTX??1-4), the two PSM? peptides (LAC?psm??hld-pTX??1-2), or the ?-toxin (LAC?psm??hld-pTX?hld) at MOI 50:1 for 2 h followed by antibiotic treatment as ,
, After various times post-infection (2 days, 5 days, 7 days and 9 days) cell supernatants were collected, centrifuged and the level of IL-1? was determined by a sandwich-ELISA (Thermofischer Life Technologies) as describe in Experimental procedures. The values are presented as concentrations in pg/mL. The differences among the groups
MG-63 or CASP1 -/-MG-63 cells were exposed to USA300 LAC (pTX?16), which carries the control plasmid, the deletion mutant LAC?psm??hld (pTX?16) and the complemented strains expressing the four PSM? peptides ,
, PSM? peptides (LAC?psm??hld-pTX??1-2), or the ?-toxin (LAC?psm??hld-pTX?hld) at MOI 50:1 for 2 h followed by antibiotic treatment as described. Six hours post-infection cells were lysed with 0.05% Triton X-100 in PBS
MG-63 or CASP1 -/-MG-63 G2 cells were grown in 12-well plates overnight, then were exposed to S. aureus SA113 strain at MOI 50:1 for 2 h followed by antibiotic treatment as described. Two hours, 6 h and 24 h post-infection cells were lysed with ,
, Experiments were performed in triplicate. Three independent assays were performed. The data are presented as means ± SD. Tukey's Honestly Significant Difference test was applied for comparison of means between the groups. P ? 0.01 (**), for the comparison of the number of internalized bacteria in CASP1 -/-MG-63 cells with those in WT MG-63 cells and P-values < 0.05 ( ? ) for the comparison of the number of internalized bacteria in CASP1 -/-MG-63 cells 6, 05% Triton X-100 in PBS, cell lysates were plated on BHI agar, and CFU were determined after overnight incubation. CFU values were normalized to 10 5 host cells
, 63 cells were grown on the slides of 12-well plates overnight, then cells were exposed to a fluorescent derivative of strain S. aureus SA113 fluorescent, which carries plasmid-encoded mCherry (red fluorescence), at MOI 50:1 for 2 h followed by antibiotic treatment as described. Six hours and 24 h postinfection cells were stained with rabbit anti-PYCARD antibody (Coger France), followed by incubation with Alexa Fluor 488 labeled goat anti-rabbit antibody, Cell Signaling Ozyme
, Phase contrast and fluorescent image of host cells bearing S. aureus were employed to demonstrate the intracellular localization of bacteria (Inserts). We have presented inset boxes
, WT MG-63 or CASP1 -/-MG-63 cells were exposed to a fluorescent derivative of S
, aureus SA113 at MOI 50:1 for 2 h followed by antibiotic treatment as described in Experimental procedures. Six hours post-infection nuclear DNA was labeled with DAPI
Reconstituted 3D images of S. aureus-infected host cells were obtained by Z-stack, showing internalized S. aureus bacteria in the cytoplasm of infected cells ,
Transmission electron micrographs of WT MG-63 or CASP1 -/-MG-63 G2 cells infected with SA113 strain at MOI 50:1 for 6 h. Cells were fixed as described in Experimental procedures. The pellets were mixed with 3% agar in sodium cacodylate, embedded in Epon-Araldite-DMP30 resin mixture and polymerized for 48 h. Sections were cut in Leica ultra microtome, stained with uranyl acetate and were analyzed with JEOL 1400 Electron Microscope (Jeol ,